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Long non-coding RNAs (lncRNAs) are ncRNA transcripts >200 nucleotides that are important genetic regulators. LncRNAs can directly regulate mRNA through a lncRNA-mRNA regulatory mode and can also regulate mRNA through competitive binding to micro (mi)RNA, which is generally known as the competitive endogenous RNA (ceRNA) network. The present study evaluated the functional roles and regulatory networks of lncRNAs in chronic glomerulonephritis (CGN). The proliferative ability of mouse glomerular mesangial cells (GMCs) induced by different concentrations of lipopolysaccharide (LPS) was assessed using the Cell Counting Kit-8 assay, and RNA sequencing (RNA-seq) was performed to identify differentially expressed lncRNAs in LPS-induced GMCs. Based on the sequencing results, six lncRNAs were selected for validation using reverse transcription-quantitative PCR (RT-qPCR). Furthermore, the lncRNA-mRNA regulatory network and the lncRNA-miRNA-mRNA ceRNA network were constructed to assess the role and mechanism of CGN-related lncRNAs. To elucidate the biological functions of lncRNAs, Gene Ontology (GO) biological process term enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed on all mRNAs involved in the lncRNA-mRNA regulatory network and in the ceRNA network. A total of 1,532 differentially expressed lncRNAs, including 594 upregulated lncRNAs and 938 downregulated lncRNAs, were identified using RNA-seq The results of RT-qPCR validation were consistent with RNA-seq results. An lncRNA-mRNA regulatory network, including 236 lncRNAs and 556 mRNAs, and a ceRNA network, including 6 lncRNAs, 18 miRNAs and 419 mRNAs, were successfully constructed. The GO biological process term enrichment and KEGG pathway enrichment analyses demonstrated that those lncRNAs were often related to inflammatory response and substance metabolism. The present study identified key CGN-related lncRNAs in LPS-induced GMCs, and further demonstrated a global view of the lncRNA-mRNA regulatory network and ceRNA network involved in CGN. These results offered novel insights into the roles of lncRNAs in the pathogenesis of CGN and identified potential diagnostic biomarkers. [ABSTRACT FROM AUTHOR]

Cancer is a serious and potentially life-threatening disease, which, despite numerous advances over several decades, remains a challenge to treat that challenging to detect at an early stage or treat during the later stages. Long noncoding RNAs are >200 nucleotides long and do not possess protein-coding capacity, instead regulating cellular processes, such as proliferation, differentiation, maturation, apoptosis, metastasis, and sugar metabolism. Several studies have shown the role of lncRNAs and glucose metabolism in regulating several key glycolytic enzymes and the activity of multiple functional signaling pathways during tumor progression. Thus, it is possible to further learn about the effects of lncRNA and glycolytic metabolism on tumor diagnosis, treatment, and prognosis through a thorough investigation of the lncRNA expression profiles and glycolytic metabolism in tumors. This may provide a novel strategy for improving the management of several types of cancer. [ABSTRACT FROM AUTHOR]

Colorectal cancer (CRC) ranks as the 3rd most common cancer globally and is the 2nd leading cause of cancer-related death. Owing to the lack of specific early symptoms and the limitations of existing early diagnostic methods, most patients with CRC are diagnosed at advanced stages. To overcome these challenges, researchers have increasingly focused on molecular biomarkers, with particular interest in long non-coding RNAs (lncRNAs). These non-protein-coding RNAs, which exceed 200 nucleotides in length, play critical roles in the development and progression of CRC. The stability and detectability of lncRNAs in the circulatory system make them promising candidate biomarkers. The analysis of circulating lncRNAs in peripheral blood represents a potential option for minimally invasive diagnostic tests based on liquid biopsy samples. The present review aimed to evaluate the efficacy of lncRNAs with altered expression levels in peripheral blood as diagnostic markers for CRC. Additionally, the clinical significance of lncRNAs as prognostic markers for this disease were summarized. [ABSTRACT FROM AUTHOR]

Aberrant expression of long non-coding RNAs (lncRNAs) serves a crucial role in the biological function of trophoblasts and contributes to preeclampsia (PE). lncRNA MIR193BHG expression is increased in PE placental tissues. In the present study, the effects of MIR193BHG on the function of trophoblasts were assessed to elucidate its underlying molecular mechanisms. The subcellular localization of MIR193BHG in HTR-8/SVneo human first-trimester extravillous trophoblast cells was determined using a fluorescent in situ hybridization assay and by conducting nucleocytoplasmic separation. The effect of MIR193BHG knockdown or overexpression on proliferation, migration, invasion and apoptosis was evaluated in vitro using Cell Counting Kit-8, wound healing, Transwell and flow cytometry assays. RNA-sequencing, Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis and protein-protein interaction network construction were subsequently performed to screen the downstream molecules regulated by MIR193BHG. Finally, rescue experiments were conducted to ascertain whether MIR193BHG influenced the biological function of trophoblasts via p53. MIR193BHG was predominantly localized in the nucleus of HTR-8/SVneo cells and overexpression of MIR193BHG significantly inhibited proliferation, migration and invasion, while increasing the rate of apoptosis of HTR-8/SVneo cells. Knockdown of MIR193BHG had the opposite effect. Furthermore, overexpression of MIR193BHG led to increases in both mRNA and protein levels of p53 compared with the control group, and knockdown of p53 rescued the effects induced by overexpression of MIR193BHG on cell proliferation, migration and invasion, while partially counteracting its effects on apoptosis of HTR-8/SVneo cells. In conclusion, the findings of the present study suggested that MIR193BHG served a critical role in progression of PE by regulating the expression of p53, and may be a novel therapeutic target for PE. [ABSTRACT FROM AUTHOR]

Long non-coding RNAs, such as homeobox A cluster antisense RNA2 (HOXA-AS2) are understood to be involved in tumor growth and development of numerous cancers. However, the role of HOXA-AS2 in the progression of human epithelial ovarian cancer (EOC) remains unclear. In the present study, the expression of HOXA-AS2 was found to be upregulated in EOC tissues compared with noncancerous tissues, and to be strongly correlated to an advanced Federation International of Gynecology and Obstetrics grade and poor prognosis. Knockdown of HOXA-AS2 in the EOC cells inhibited cell proliferation, invasion and migration, as well as inducing cell apoptosis. The ENCORI database was used to screen the microRNAs (miRNAs/miRs) that bound to HOXA-AS2, and one was tested using RNA pull-down and luciferase reporter assays. It was demonstrated that HOXA-AS2 functioned through the competing endogenous RNA mechanism to regulate miR-372. It was also demonstrated that the downregulation of miR-372 reversed the inhibitory effects of the knockdown of HOXA-AS2 in EOC cells. These results indicated that HOXA-AS2 promoted EOC progression by regulating the miR-372, which suggests that HOXA-AS2 may be a therapy target for EOC. [ABSTRACT FROM AUTHOR]

Progressive liver fibrosis is the most common phenotype in biliary atresia (BA). A number of pathways contribute to the fibrosis process so comprehensive understanding the mechanisms of liver fibrosis in BA will pave the way to improve patient's outcome after operation. In this study, the differentially expressed profiles of mRNAs and long non-coding RNAs from BA and choledochal cyst (CC) liver tissues were investigated and analyzed, which may provide potential clues to clarify hepatofibrosis mechanism in BA. A total of two BA and two CC liver tissue specimens were collected, the expression level of mRNAs and lncRNAs was detected by RNA sequencing. Differentially expressed mRNAs (DEmRNAs) were functionally annotated and protein-protein interaction networks (PPI) was established to predict the biological roles and interactive relationships. Differentially expressed lncRNAs (DElncRNAs) nearby targeted DEmRNA network and DElncRNA-DEmRNA co-expression network were constructed to further explore the roles of DElncRNAs in BA pathogenesis. The expression profiles of significant DEmRNAs were validated in Gene Expression Omnibus database. A total of 2,086 DEmRNAs and 184 DElncRNAs between BA and CC liver tissues were obtained. DEmRNAs were enriched in 521 Gene Ontology terms and 71 Kyoto Encyclopedia of Genes and Genomes terms which were mainly biological processes and metabolic pathways related to immune response and inflammatory response. A total of five hub proteins (TYRO protein tyrosine kinase binding protein, C-X-C motif chemokine ligand 8, pleckstrin, Toll-like receptor 8 and C-C motif chemokine receptor 5) were found in the PPI networks. A total of 31 DElncRNA-nearby-targeted DEmRNA pairs and 2,337 DElncRNA-DEmRNA co-expression pairs were obtained. The expression of DEmRNAs obtained from RNA sequencing were verified in GSE46960 dataset, generally. The present study identified key genes and lncRNAs participated in BA associated liver fibrosis, which may present a new avenue for understanding the patho-mechanism for hepatic fibrosis in BA. [ABSTRACT FROM AUTHOR]

Long non-coding RNAs (lncRNAs) have been confirmed to be connected with tumor proliferation, apoptosis, metastasis and recurrence. Previous studies have indicated that lncRNA calcium voltage-gated channel subunit a1 G (CACNA1G)-antisense 1 (AS1) can function as a pro-oncogene in several types of cancer. However, the specific role and mechanism of CACNA1G-AS1 have not been fully elucidated in human diffuse large B cell lymphoma (DLBCL). In the present study, CACNA1G-AS1 expression was verified in DLBCL tissues and cells by reverse transcription-quantitative PCR, and the relationship between CACNA1G-AS1 and microRNA (miR)-3160-5p was confirmed using luciferase reporter assays. After CACNA1G-AS1-knockdown and miR-3160-5p-overexpression, MTT, colony formation and flow cytometry assays were conducted to assess the changes in the cytotoxicity and apoptosis of OCI-Ly10 and SUDHL-4 cells. In addition, in vivo experiments were performed to determine the impact of CACNA1G-AS1-knockdown on tumor growth and apoptosis. It was revealed that CACNA1G-AS1 was highly expressed in DLBCL tissues and cells and that expression of CACNA1G-AS1 was associated with the clinical stage of DLBCL. Functionally, CACNA1G-AS1-knockdown was demonstrated to increase cytotoxicity and expedite apoptosis in DLBCL cells in vitro and in vivo. In addition, CACNA1G-AS1 could downregulate miR-3160-5p by targeting binding in DLBCL cells. Overexpression of miR-3160-5p had the same effects on the cytotoxicity and apoptosis of DLBCL cells as CACNA1G-AS1-knockdown. Overall, the present study revealed that CACNA1G-AS1-knockdown and miR-3160-5p-overexpression could prevent DLBCL carcinogenesis, which might provide novel therapeutic targets for DLBCL. [ABSTRACT FROM AUTHOR]

Long non-coding (lnc)RNAs serve a pivotal role as regulatory factors in carcinogenesis. The present study aimed to assess the involvement of the lncRNA progression and angiogenesis-associated RNA in hepatocellular carcinoma (PAARH) in liver cancer, along with the associated underlying mechanism. Through the use of reverse transcription-quantitative (RT-q)PCR, differences in the expression levels of PAARH in HepG2, HEP3B2.1.7, HCCLM3, Huh-7 and MHCC97-H liver cancer cell lines and THLE-2 epithelial cell lines were evaluated. The liver cancer cell line with the greatest, significantly different, level of expression relative to the normal liver cell line was selected for subsequent experiments. Using ENCORI database, the putative target genes of the microRNA (miR) miR-6512-3p were predicted. Cells were then transfected with lentiviruses carrying short-hairpin-PAARH to interfere with PAARH expression. Subsequently, HepG2 liver cancer cells were transfected with a miR-6512-3p mimic and an inhibitor, and the expression levels of miR-6512-3p and the LIM and SH3 domain protein 1 (LASP1) in cells were assessed using RT-qPCR analysis. Cell proliferation was subsequently evaluated using colony formation assays, and immunofluorescence and western blotting were used to assess the expression level of LASP1 in transfected cells. The binding interaction between miR-6512-3p and LASP1 was further evaluated using a dual-luciferase reporter gene assay. Liver cancer cells were found to exhibit higher expression levels of PAARH compared with normal liver cells. Following PAARH interference, the expression level of miR-6512-3p was significantly increased, whereas that of LASP1 was significantly decreased, resulting in a reduction in cell proliferation. In liver cancer cells, miR-6512-3p overexpression led to a significant reduction in the LASP1 level and reduced proliferation, whereas suppressing miR-6512-3p led to a significant increase in LASP1 levels and increased proliferation. Additionally, the inhibition of miR-6512-3p caused the states of low LASP1 expression and reduced cell proliferation to be reversed. LASP1, a recently identified target gene of miR-6512-3p, was demonstrated to be suppressed by miR-6512-3p overexpression, thereby inhibiting liver cancer cell proliferation. Taken together, the findings of the present study demonstrate that the lncRNA PAARH may enhance liver cancer cell proliferation by engaging miR-6512-3p to target LASP1. [ABSTRACT FROM AUTHOR]

Ultraviolet (UV) is divided into UVA (long-wave, 320-400 nm), UVB (middle-wave, 280-320 nm) and UVC (short-wave, 100-280 nm) based on wavelength. UV radiation (UVR) from sunlight (UVA + UVB) is a major cause of skin photodamage including skin inflammation, aging and pigmentation. Accidental exposure to UVC burns the skin and induces skin cancer. In addition to the skin, UV radiation can also impair visual function. Non-coding RNAs (ncRNAs) are a class of functional RNAs that do not have coding activity but can control cellular processes at the post-transcriptional level, including microRNA (miRNA), long non-coding RNA (lncRNA) and circulatory RNA (circRNA). Through a review of the literature, it was determined that UVR can affect the expression of various ncRNAs, and that this regulation may be wavelength specific. Functionally, ncRNAs participate in the regulation of photodamage through various pathways and play pathogenic or protective regulatory roles. In addition, ncRNAs that are upregulated or downregulated by UVR can serve as biomarkers for UV-induced diseases, aiding in diagnosis and prognosis assessment. Therapeutic strategies targeting ncRNAs, including the use of natural drugs and their extracts, have shown protective effects against UV-induced photodamage. In the present review, an extensive summarization of previous studies was performed and the role and mechanism of ncRNAs in UV-induced radiation effects was reviewed to aid in the diagnosis and treatment of UV-related diseases. [ABSTRACT FROM AUTHOR]

Esophageal cancer (EC) is a common form of malignant tumor in the digestive system that is classified into two types: Esophageal squamous cell carcinomas (ESCC) and esophageal adenocarcinoma. ESCC is known for its early onset of symptoms, which can be difficult to identify, as well as its rapid progression and tendency to develop drug resistance to chemotherapy and radiotherapy. These factors contribute to the high incidence of disease and low cure rate. Therefore, a diagnostic biomarker and therapeutic target need to be identified for ESCC. Non-coding RNAs (ncRNAs) are a class of molecules that are transcribed from DNA but do not encode proteins. Initially, ncRNAs were considered to be non-functional segments generated during transcription. However, with advancements in high-throughput sequencing technologies in recent years, ncRNAs have been associated with poor prognosis, drug resistance and progression of ESCC. The present study provides a comprehensive overview of the biogenesis, characteristics and functions of ncRNAs, particularly focusing on microRNA, long ncRNAs and circular RNAs. Furthermore, the ncRNAs that could potentially be used as diagnostic biomarkers and therapeutic targets for ESCC are summarized to highlight their application value and prospects in ESCC. [ABSTRACT FROM AUTHOR]

Glucose metabolism, as a novel theory to explain tumor cell behavior, has been intensively studied in various tumors. The present study explored the long non-coding RNAs (lncRNAs) related to glycolysis in grade II–III glioma, aiming to provide a promising target for further research. Pearson correlation analysis was used to identify glycolysis-related lncRNAs. Univariate/multivariate Cox regression analysis and the Least Absolute Shrinkage and Selection Operator algorithm were applied to identify glycolysis-related lncRNAs to construct a prognosis prediction model. Subsequently, multi-dimensional evaluations were used to verify whether the risk model could predict the prognosis and survival rate of patients with grade II–III glioma. Finally, it was verified by functional experiments. The present study finally identified seven glycolysis-related lncRNAs (CRNDE, AC022034.1, RHOQ-AS1, AL159169.2, AL133215.2, AC007098.1 and LINC02587) to construct a prognosis prediction model. The present study further investigated the underlying immune microenvironment, somatic landscape and functional enrichment pathways. Additionally, individualized immunotherapeutic strategies and candidate compounds were identified to guide clinical treatment. The experimental results demonstrated that CRNDE could increase the proliferation of SHG-44 cells. In conclusion, a large sample of human grade II–III glioma in The Cancer Genome Atlas database was used to construct a risk model using glycolysis-related lncRNAs to predict the prognosis of patients with grade II–III glioma. [ABSTRACT FROM AUTHOR]

The present study aimed to investigate the differential expression of long non-coding RNAs (lncRNAs) in rheumatoid arthritis (RA). High-throughput gene sequencing technology was used to detect the expression of lncRNA and mRNA in three patients with RA (RA group) and normal controls (NC group). A Bioinformatics analysis was used to assess the effects of differentially expressed mRNAs on signaling pathways and biological functions. The selected dysregulated lncRNAs were verified by reverse transcription-quantitative (RT-q)PCR in the peripheral blood mononuclear cells (PBMCs) of patients with RA and age- and sex-matched controls. A correlation analysis was used to analyze the relationship between lncRNAs and clinical indexes. From the lncRNA sequencing data, significantly differentially expressed lncRNAs between the RA and NC groups were identified by a fold change ≥2 and P<0.05. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analysis suggested that the differentially expressed mRNAs were mainly involved in organelle composition, intracellular regulation, signaling pathways, cancer, virus and inflammation. A total of four of these lncRNAs were confirmed by RT-qPCR to be significantly differentially expressed (LINC00304, MIR503HG, LINC01504 and FAM95B1). Through the correlation analysis, it was confirmed that there was a strong correlation between these lncRNAs and clinical laboratory indicators and indexes such as course of disease, arthrocele and joint tenderness. Overall, the present results suggested that the expression levels of LINC00304, MIR503HG, LINC01504 and FAM95B1 in PBMCs from patients with RA may serve as potential biomarkers for RA diagnosis, influencing the occurrence and progress of RA. [ABSTRACT FROM AUTHOR]

Oral squamous cell carcinoma (OSCC), characterized by a high recurrence rate, a poor prognosis and high morbidity, is the most prevalent malignancy of the oral cavity. The aberrant expression of long non-coding RNAs (lncRNAs) may lead to the development of various diseases, including cancer. Delayed diagnosis is the main reason for the poor prognosis. Therefore, the present study aimed to investigate the differential expression profiles of plasma lncRNAs in OSCC in order to screen target lncRNAs as biomarkers for the early diagnosis and staging of OSCC. The expression profiles of lncRNAs and mRNAs in OSCC were analyzed by microarray analysis. A total of 14 candidate lncRNAs were selected and analyzed using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) using the array homologous samples. Subsequently, 4 target lncRNAs were measured by RT-qPCR in a large cohort, including 28 cases with TNM I/II [early-stage squamous cell carcinoma (ESCC) group], 36 cases with TNM III/IV [advanced-stage squamous cell carcinoma (ASCC) group], 16 cases with dysplasia [oral premalignant lesion (OPL) group] and 16 healthy controls (H group). Receiver operating characteristic (ROC) curves and logistic regression analysis were used to evaluate the diagnostic effects of the combined lncRNAs. In total, 6,606 differentially expressed lncRNAs and 4,196 mRNAs were identified in OSCC. The expression trend of the 14 candidate lncRNAs was consistent with the microarray data. The expression level of ENST00000412740, NR_131012, ENST00000588803 and NR_038323 exhibited significant differences in the H, OPL, ESCC and ASCC groups (P<0.05). ROC curve and logistic regression analyses revealed that the diagnostic efficacy of the combined lncRNAs was more prominent than that of a single lncRNA, particularly in the ESCC and ASCC groups. In conclusion, the present study identified the differential expression profiles of plasma lncRNAs in OSCC and demonstrated that ENST00000412740, NR_131012, ENST00000588803 and NR_038323 may be promising biomarkers for the early diagnosis and staging of OSCC. These findings may provide novel targets for the early diagnosis and staging of OSCC, which may provide an objective basis for clinical decision-making. [ABSTRACT FROM AUTHOR]

Long non-coding RNAs (lncRNAs) affect atherosclerosis by regulating the physiological and pathological processes of endothelial cells; however, the role of lncRNA WEE2 antisense RNA 1 (WEE2‑AS1) in arteriosclerosis obliterans (ASO) is not completely understood. The present study aimed to explore the function of lncRNA WEE2‑AS1 in human vascular endothelial cells. The results indicated that lncRNA WEE2‑AS1 was significantly elevated in plasma and artery tissue samples of patients with ASO compared with healthy controls. The fluorescence in situ hybridization results suggested that lncRNA WEE2‑AS1 was expressed in the cytoplasm and nuclei of primary human umbilical vein endothelial cells (HUVECs). The Cell Counting Kit-8 assay results suggested that lncRNA WEE2‑AS1 knockdown significantly promoted HUVEC viability, whereas lncRNA WEE2‑AS1 overexpression inhibited HUVEC viability compared with the negative control groups. Furthermore, analysis of the cell cycle by flow cytometry indicated that lncRNA WEE2‑AS1 knockdown significantly decreased the proportion of cells in the G0/G1 phase and significantly increased the proportion of cells in the G2/M phase compared with the negative control group. However, lncRNA WEE2‑AS1 overexpression had no significant effect on cell cycle distribution compared with the negative control group. The western blotting results indicated that lncRNA WEE2‑AS1 knockdown significantly reduced the expression levels of phosphorylated cyclin dependent kinase 1, WEE1 homolog 2 and myelin transcription factor 1, but increased the expression level of cell division cycle 25B compared with the negative control group. lncRNA WEE2‑AS1 overexpression displayed the opposite effect on protein expression. Collectively, the present study suggested that lncRNA WEE2‑AS1 was significantly upregulated in ASO and may serve a role in regulating human vascular endothelial cell viability. Further investigation into lncRNA WEE2‑AS1 may broaden the current understanding of the molecular mechanism underlying ASO, and aid with the identification of specific probes and precise targeted drugs for the diagnosis and treatment of ASO. [ABSTRACT FROM AUTHOR]

Non-coding RNAs (ncRNAs) have been previously reported to serve an important role in transcription. In addition, several studies have revealed that long ncRNAs (lncRNAs) have a crucial role in human diseases. However, the association between lncRNAs and inflammation-induced intestinal macrophages in the intestinal mucosal barrier has remained elusive. In the present study, intestinal macrophages from healthy Sprague Dawley rats were divided into two groups: The experimental group, consisting of intestinal macrophages treated with 1 mg/l lipopolysaccharide (LPS) and the control group, composed of untreated cells. Differentially expressed (DE) lncRNAs and mRNAs between the control and experimental groups were identified using microarray profiling. The levels of DE mRNAs and lncRNAs were measured by reverse transcription-quantitative PCR (RT-qPCR). Furthermore, Gene Ontology (GO) and pathway enrichment analyses of DE mRNAs and lncRNAs were performed. To identify core regulatory factors among DE lncRNAs and mRNAs, a lncRNA-mRNA network was constructed. A total of 357 DE lncRNAs and 542 DE mRNAs between the LPS-treated and untreated groups were identified (fold-change >1.5; P<0.05). In addition, selected microarray data were confirmed by RT-qPCR. GO analysis of the DE mRNAs indicated that the biological functions of the upregulated mRNAs included inflammatory response, immune response, metabolic process and signal transduction, whereas those of the downregulated mRNAs were metabolic process, cell cycle, apoptosis and inflammatory response. In addition, pathway enrichment analysis of the upregulated mRNAs revealed that the most enriched pathways were the NF-κB signaling pathway, B-cell receptor signaling pathway and apoptosis, while the downregulated mRNAs were significantly involved in metabolic pathways, the phosphatidylinositol signaling system, cytokine-cytokine receptor interaction and the Toll-like receptor signaling pathway. The lncRNA-mRNA co-expression network suggested that lncRNAs NONMMUT024673 and NONMMUT062258 may have an important role in LPS-induced intestinal macrophages. The present study identified the DE profiles between LPS- and non-LPS-treated intestinal macrophages. These DE lncRNAs and mRNAs may be used as potential targets for attenuating excessive inflammatory response in intestinal mucosal barrier dysfunction. [ABSTRACT FROM AUTHOR]

Renal cell carcinoma (RCC) is a primary malignant kidney cancer subtype. It has been suggested that long non-coding RNAs (lncRNAs) serve important roles in the progression of kidney cancer. In fact, the lncRNA small nucleolar RNA host gene 12 (SNHG12) was discovered to be overexpressed in various types of cancer. However, to the best of our knowledge, the role of SNHG12 in RCC remains unclear. The present study aimed to investigate the function of SNHG12 and its underlying molecular mechanism of action in RCC. In patient samples and datasets from The Cancer Genome Atlas. Reverse transcription-quantitative PCR, demonstrated that SNHG12 expression levels were upregulated in RCC tumor tissues, but not in normal kidney tissues. SNHG12 upregulation was also observed in RCC cell lines. Kaplan-Meier survival analysis indicated a poor prognosis for those patients with RCC who had upregulated SNHG12 expression levels. Following lentivirus transduction, SNHG12 was successfully knocked down (validated by western blot analysis) and cell migration and invasion assays were performed. SNHG12 knockdown markedly inhibited cell viability and invasion, while increasing apoptosis in both A498 and 786O cell lines. The results of the luciferase reporter assay suggested that SNHG12 exerted its role by sponging microRNA (miR)-200c-5p, which led to the upregulation of its target gene, collagen type XI α1 chain (COL11A1). This was further validated, as miR-200c-5p inhibition reduced the effects of SNHG12 downregulation on cell viability and apoptosis, without affecting SNHG12 expression levels. Furthermore, the findings indicated that SNHG12 may partially exert its role through COL11A1, which was also upregulated in RCC. In conclusion, the results of the present study suggested that the SNHG12/miR-200c-5p/COL11A1 axis may be crucial for RCC progression, which provided an insight into potential therapeutic strategies for RCC treatment. [ABSTRACT FROM AUTHOR]

Oral squamous cell carcinoma (OSCC) is the most common malignant tumor of the oral cavity. Emerging evidence indicates that long non-coding (lnc)RNAs play a key role in the cellular processes of tumor cells, including glycolysis, growth and movement. Here, the purpose of this study was to explore the biological functions and potential mechanism of lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) in OSCC. OSCC tissues and adjacent matched paraneoplastic normal tissues were collected from 20 OSCC patients. The expression of MALAT1 and miR-101 in OSCC tissues and cell lines (HSC3, SCC9, SCC15 and SCC25) were determined by real-time-polymerase chain reaction (qPCR). Caspase-3, xaspase-8 and EZH2 protein levels were determined by western blot analysis. MALAT1-mediated miRNAs were verified by bioinformatics analysis of StarBase and Luciferase reporter assay. Cell Counting Kit-8 (CCK-8) and Transwell assays were used for investigating MALAT1 effect on cell proliferation and invasion in the OSCC cells. qPCR analysis indicated that MALAT1 expression was obviously increased, and miR-101 was decreased in the OSCC tissues and cell lines. Functional studies revealed that overexpression of MALAT1 promoted OSCC cell proliferation and invasion. Further experiments revealed that miR-101 was a target of MALAT1 and that the miR-101 inhibitor abolished the effect of MALAT1 on OSCC cell proliferation and invasion. Enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) acted as a downstream effecter of MALAT1 in the OSCC cells. Collectively, these findings revealed that upregulation of MALAT1 facilitated OSCC proliferation and invasion by targeting the miR-101/EZH2 axis. [ABSTRACT FROM AUTHOR]

Cervical carcinoma expressed PCNA regulatory long non-coding (lnc)RNA (CCEPR) has recently been reported to play oncogenic roles in some common types of human cancer. However, the clinical significance of CCEPR mRNA expression levels in esophageal squamous cell carcinoma (ESCC) and the exact function of CCEPR in regulating the malignant phenotypes of ESCC cells have not been previously investigated. In the present study, CCEPR mRNA expression level was upregulated in ESCC tissues and cell lines, and overexpression of CCEPR was associated with advanced TNM stage, lymph node metastasis, and poor prognosis in ESCC. In vitro experiments showed that silencing CCEPR mRNA expression levels significantly suppressed the proliferation, migration, and invasion of ESCC cells, while inducing ESCC cell apoptosis. Furthermore, inhibition of CCEPR decreased the protein expression levels of matrix metalloproteinase (MMP)2 and MMP9 and inhibited epithelial-mesenchymal transition in ESCC cells. In conclusion, the results showed that CCEPR plays an oncogenic role in ESCC and suggests that CCEPR could be used as a potential therapeutic target for ESCC treatment. [ABSTRACT FROM AUTHOR]

Several studies have reported a prognostic role of the long non-coding RNA (lncRNA) cancer susceptibility candidate 9 (CASC9) in various cancer types, but its clinical significance has remained inconclusive. The aim of the present meta-analysis was to evaluate the impact of CASC9 expression on the prognosis and clinicopathological features of patients with cancer patients. The PubMed, Embase, Cochrane Library and Web of Science databases were searched for relevant literature and eight studies, including 565 patients with cancer, were selected. The quality of these studies was appraised with the Newcastle-Ottawa Scale (NOS) and the association between CASC9 expression and prognosis or clinicopathological features was analyzed. Patients with high expression levels of CASC9 in their tumor tissues had a lower overall survival rate compared with those in the low CASC9 expression group (hazard ratio=2.25, 95% CI: 1.60-3.17, P<0.001). Furthermore, elevated CASC9 expression was significantly associated with deeper tumor invasion [odds ratio (OR)=2.66, 95% CI: 1.72-4.14, P<0.001], poor tumor differentiation (OR=2.44, 95% CI: 1.24-4.78, P=0.009), lymph node metastasis (OR=3.42, 95% CI: 1.98-5.92, P<0.001) and advanced clinical stage (OR=3.21, 95% CI: 2.21-4.66, P<0.001). In conclusion, CASC9 is a promising biomarker for predicting the prognosis of cancer patients and should be validated in the clinic. [ABSTRACT FROM AUTHOR]

Long non-coding RNA (lncRNA) ZNFX1 antisense RNA 1 (ZFAS1) is upregulated in acute myocardial infarction; however, the role of ZFAS1 in myocardial ischemia/reperfusion (I/R) injury remains unknown. The present study aimed to detect microRNA (miR)-590-3p expression levels in cardiomyocytes subjected to I/R, and to investigate the effects of ZFAS1 on myocardial I/R injury. An in vitro model of I/R injury was established using rat H9c2 cardiomyocytes exposed to hypoxia/reoxygenation (H/R). It was demonstrated that ZFAS1 was upregulated and miR-590-3p was downregulated in the in vitro model of cardiac I/R injury. Western blotting results indicated that the protein expression levels of p50, tumor necrosis factor-α (TNF-α), interleukin (IL)-6, Bax and cleaved caspase-3 were upregulated, and the expression levels of Bcl-2 and pro-caspase-3 were downregulated. Flow cytometry results revealed that downregulation of ZFAS1 reduced H/R-induced apoptosis in H9c2 cells. In addition, downregulation of ZFAS1 significantly increased the expression of miR-590-3p, and p50 was identified as a target gene of miR-590-3p. Furthermore, with 12 h of hypoxia followed by 2 h of reoxygenation in H9c2 cells, ZFAS1 knockdown increased the expression levels of miR-590-3p, Bax and cleaved-caspase-3, and decreased the expression levels of Bcl-2 and pro-caspase-3. It was also found that the miR-590-3p-mimic transfection increased the expression levels of Bax and cleaved-caspase-3, and decreased the protein expression levels of p50, TNF-α, IL-6, Bcl-2 and pro-caspase-3. In addition, TNF-α treatment induced apoptosis of H9c2 cells, and the changes in Bax, Bcl-2, cleaved-caspase-3 and pro-caspase-3 expression levels in a dose-dependent manner. Collectively, the present results suggested that ZFAS1 was upregulated in H9c2 cells subjected to I/R injury, and that ZFAS1 knockdown protected against I/R-induced myocardial cell apoptosis by directly interacting with miR-590-3p, via the NF-κB pathway. [ABSTRACT FROM AUTHOR]

Accumulating evidence has indicated that long non-coding RNAs (lncRNAs) have crucial roles in wound healing and that vascular lesions in diabetic wounds are frequently difficult to heal. However, the role of angiogenesis pathway-associated lncRNAs in wound healing in diabetic patients has remained to be fully elucidated. In the present study, human skin fibroblasts were cultured under high-glucose conditions in vitro to mimic a diabetic environment and the angiogenesis pathway-associated lncRNA expression profile in the high- and normal-glucose groups was examined. The microarray data indicated that 14 lncRNAs and 22 mRNAs were differentially expressed. Several candidate lncRNAs and mRNAs were then analyzed by reverse transcription-quantitative PCR and the results were consistent with the microarray data. Furthermore, the University of California Santa Cruz Genome Browser was used to identify mRNAs linked to angiogenesis pathways near the transcriptional region of lncRNAs. The results suggested that lncRNAs RP4-791C19.1 and CTD-2589O24.1 may act on their target genes epidermal growth factor receptor and p21 (RAC1) activated kinase 1, respectively, as enhancers and cis-regulate their expression. Therefore, the present study confirmed that several angiogenesis pathway-associated lncRNAs were differentially expressed under high-glucose conditions, which may have a key role in wound healing in patients with diabetes. [ABSTRACT FROM AUTHOR]

Chronic obstructive pulmonary disease (COPD) is a pathological inflammatory condition of the lungs that is associated with high rates of mortality. Although long non-coding RNAs (lncRNAs) serve a role in lung diseases, their functions in COPD pathogenesis are relatively unknown. The present study aimed to assess the role of differentially expressed lncRNAs in COPD. Expression profile analysis of six lncRNAs in age-matched COPD and non-COPD tissues were conducted. Among the six tested lncRNAs, metastasis-associated in lung adenocarcinoma transcript 1 (MALAT1) was the most consistently overexpressed in COPD lung tissue specimens. To model COPD in vitro, human lung fibroblasts were treated with transforming growth factor-β (TGF-β) and MALAT1 was knocked down by small interfering RNA. This promoted cell viability and concurrently inhibited the expression of mesenchymal proteins, fibronectin and α-smooth muscle actin. In COPD, cell senescence is linked to the activation of mammalian target of rapamycin complex 1 (mTORC1). Upon gene silencing of MALAT1 in non-TGF-β-treated cells, cells demonstrated constitutive activation of mTORC1, which was assessed by the protein expression levels of mTORC1 substrate S6 kinase (S6K1). By contrast, upon MALAT1 silencing in the TGF-β-treated cells, mTORC1 activation was not suppressed, despite the mesenchymal cell markers protein expression levels being downregulated. Thus, lncRNA MALAT1 may represent a potent biomarker in COPD patients and may act as a target for both diagnostic and therapeutic purposes. [ABSTRACT FROM AUTHOR]

Osteosarcoma is a malignant tumor that occurs in children and adolescents. Although treatments for osteosarcoma have improved, the likelihood of survival remains low for most patients with metastasis and recurrence. Elucidating the mechanism underlying the development of osteosarcoma and chemotherapy resistance will be important to improve diagnosis and treatment. Long non-coding RNAs (lncRNAs), which are longer than 200 nucleotides in length and do not encode for proteins, have been shown to play a regulatory role in the occurrence and development of osteosarcoma, and are expected to serve as biomarkers and molecular targets. This review discusses the progress in the study of the role of lncRNAs in osteosarcoma, and highlights the recent developments in this field. [ABSTRACT FROM AUTHOR]

Long non-coding RNAs (lncRNAs) constitute a group of >200-nucleotide ncRNA molecules. lncRNAs regulate several cell functions, such as proliferation, apoptosis, invasion and metastasis. Meanwhile, lncRNAs are abnormally expressed in human malignancies, where they suppress or promote tumor growth. The present study focused on growth arrest-specific transcript 5 (GAS5), a well-known lncRNA that acts as a tumor suppressor but is suppressed in multiple types of cancer, including mammary carcinoma, prostate cancer, colorectal cancer, gastric cancer, melanoma, esophageal squamous cell carcinoma, lung cancer, ovarian cancer, cervical cancer, gliomas, osteosarcoma, pancreatic cancer, bladder cancer, kidney cancer, papillary thyroid carcinoma, neuroblastoma, endometrial cancer and liver cancer. Notably, GAS5 is overexpressed in liver cancer, potentially functioning as an oncogene. In the present study, the diagnostic and therapeutic roles of GAS5 in different tumors were reviewed, with a summary of the potential clinical application of the lncRNA, which may help identify novel study directions for GAS5. [ABSTRACT FROM AUTHOR]

Resveratrol (RSV) and long non-coding RNAs (lncRNAs) play a role in the treatment of diabetes; however, the mechanism by which resveratrol regulates insulin resistance via lncRNAs is currently unknown. The present study aimed to determine the lncRNA expression level profile in mice following resveratrol treatment to improve insulin resistance using high-throughput sequencing technology. C57BL/6J mice were fed a high-fat diet for 8 weeks to develop an insulin resistance model, followed by treatment with or without RSV for 6 weeks before high-throughput sequencing. Following RSV treatment, 28 and 30 lncRNAs were up- and downregulated, respectively; eight lncRNAs were randomly selected and evaluated using reverse transcription-quantitative PCR, which showed results consistent with the sequencing analysis. Pathway analysis demonstrated that the insulin signaling pathway enrichment score was the highest, and identified two lncRNAs, NONMMUT058999.2 and NONMMUT051901.2, consistent with the protein-encoding genes SOCS3 and G6PC, respectively. Similar expression level patterns were observed for SOCS3 and G6PC, suggesting that RSV improves insulin resistance by modulating lncRNAs. RSV decreased the expression levels of SOCS3, FOXO1, G6PC and PEPCK in mice. The same results were observed following knockdown of NONMMUT058999.2 in cells. The present study provides a new biomarker or intervention target for RSV in the treatment of diabetes, and a new perspective for understanding the hypoglycemic mechanism of RSV. [ABSTRACT FROM AUTHOR]

Acute myelocytic leukemia (AML) is a frequent type of acute leukemia. The present study was performed to build a risk score system for the prognostic prediction of AML. AML RNA-sequencing data from samples from 111 children were downloaded from The Cancer Genome Atlas database. Using the DEseq and edgeR packages, the differentially expressed long non-coding RNAs (DE-lncRNAs) between bad and good prognosis groups were identified. A survival package was used to screen prognosis-associated lncRNAs and clinical factors. The optimal lncRNA combination was selected using the penalized package, and the risk-score system was built and evaluated. After the lncRNA-mRNA expression correlation network was constructed, the potential pathways involving the key lncRNAs were enriched using Gene Set Enrichment Analysis. Among the 61 DE-lncRNAs, 48 lncRNAs were significantly associated with prognosis. Relapse was an independent prognostic factor. The optimal 14-lncRNA risk score system was constructed. After 730 differentially expressed mRNAs were identified between the good and bad prognosis groups divided using a prognostic index, the lncRNA-mRNA expression correlation network was constructed. Enrichment analysis showed that semaphorin-3C [SEMA3C; regulated by probable leucine-tRNA ligase, mitochondrial (LARS2-AS1)] and secreted frizzled-related protein 5 [SFRP5; mediated by WASH complex subunit 5 (WASHC5)-antisense RNA 1 (AS1)] were involved in axon guidance and the Wnt signaling pathway, respectively. A 14-lncRNA (including paired box protein Pax8-AS1 and MYB AS1) risk-score system might be effective in predicting the prognosis of AML. Axon guidance (involving SEMA3C and LARS2-AS1) and the Wnt signaling pathway (involving SFRP5 and WASHC5-AS1) might be two important pathways affecting the prognosis of AML. [ABSTRACT FROM AUTHOR]

The present study aimed to investigate the implication of long non-coding RNA (lncRNA) expression profiles in post-menopausal osteoporosis (PMOP). A total of 10 patients with PMOP and 10 age-matched healthy post-menopausal females as controls were consecutively enrolled. Their peripheral blood mononuclear cells were obtained and lncRNA as well as mRNA expression profiles were detected by RNA sequencing, followed by bioinformatics analyses. The lncRNA expression profiles were able to distinguish patients with PMOP from controls based on principal component analysis and heatmap analysis. In total, 254 upregulated lncRNAs and 359 downregulated lncRNAs were identified in patients with PMOP vs. controls. The top 5 upregulated lncRNAs were RP11-704M14.1, RP11-754N21.1, RP11-408E5.5, ANKRD26P3 and TPTEP1. The top 5 downregulated lncRNAs were RP11-310E22.4, RP11-326K13.4, FABP5P1, SERPINB9P1 and RPL13P2. Based on the interaction of dysregulated lncRNAs and mRNAs by RNA sequencing, functional annotations were then performed. Gene Ontology enrichment analysis revealed that the dysregulated lncRNAs were enriched in terms including apoptotic process and positive regulation of NF-κB transaction, and Kyoto Encyclopedia of Genes and Genomes analysis suggested enrichment in PMOP-associated signaling pathways, including osteoclast differentiation, tumor necrosis factor signaling pathway and mitogen-activated protein kinase signaling pathway. In addition, the regulatory network and circos graph further indicated the implication of lncRNA expression profiles in PMOP via interactions with mRNAs. In conclusion, the present study suggested that aberrant lncRNA expression is deeply involved in the pathogenesis of PMOP by affecting osteoclast differentiation, inflammation and apoptotic processes. [ABSTRACT FROM AUTHOR]

Hypertrophic cardiomyopathy (HCM) is an autosomal dominant disease that affects 1 in every 200 people in the general population, leading to cardiac ischemia, heart failure and increased risk of sudden death. Recently, accumulating evidence has suggested that long noncoding RNAs (lncRNAs) may serve specific roles in various biological processes and participate in the pathology of various diseases, including HCM. Although a large number of lncRNAs have been detected, the functions of lncRNAs in HCM are still unknown. In the present study, a global triple network based on competitive endogenous RNA (ceRNA) theory was constructed using data from the National Center for Biotechnology Information Gene Expression Omnibus. Furthermore, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses of mRNAs in the lncRNA-microRNA (miRNA)-mRNA network were performed using the Cytoscape plugins, BiNGO and Database. The lncRNA-miRNA-mRNA network was composed of 30 lncRNA nodes, 94 mRNA nodes and 8 miRNA nodes. Subsequently, hub nodes and the number of relationship pairs were analyzed and showed that 5 lncRNAs (ENST00000597346.1, ENST00000458178.1, ENST00000544461.1, ENST00000567093.1 and ENST00000571219.1) were closely related to HCM. Cluster module analysis and Random Walk with Restart of the ceRNA network further confirmed the potential role of two lncRNAs (ENST00000458178.1 and ENST00000567093.1) in HCM. The present study provides a new strategy for identifying potential pathways associated with HCM or other diseases. Furthermore, lncRNA-miRNA pairs may be regarded as candidate diagnostic biomarkers or potential therapeutic targets for HCM. [ABSTRACT FROM AUTHOR]

Cervical cancer is a common malignant disease that poses a serious health threat to women worldwide. Growing research efforts have focused on protein-coding and non-coding RNAs involved in the tumorigenesis and prognosis of various types of cancer. The potential molecular mechanisms and the interaction among long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and mRNAs require further investigation in cervical cancer. In the present study, lncRNA, miRNA, and mRNA expression profiles of 304 primary tumor tissues from patients with cervical cancer and 3 solid normal tissues from The Cancer Genome Atlas (TCGA) dataset were studied via RNA sequencing (RNA-seq). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed using R package clusterProfiler to annotate the principal functions of differentially expressed (DE) mRNAs. Kaplan-Meier analysis was also conducted to investigate the effects of DElncRNAs, DEmiRNAs, and DEmRNAs on overall survival. A total of 2,255 mRNAs, 133 miRNAs, and 150 lncRNAs that were differentially expressed were identified with a threshold of P<0.05 and |fold change (FC)|>2. Functional enrichment analysis indicated that DEmRNAs were enriched in cancer-associated KEGG pathways. Furthermore, 255 mRNAs, 15 miRNAs, and 12 lncRNAs that were significantly associated with overall survival in cervical carcinoma were also identified. Importantly, an miRNA-mediated competitive endogenous RNA (ceRNA) network was successfully constructed based on the expression profiles of DElncRNAs and DEmRNAs. More importantly, it was found that the lncRNA EPB41L4A-AS1 may function as a pivotal regulator in carcinoma of the uterine cervix. Taken together, the present study has provided novel insights into investigating the potential mechanisms underlying tumorigenesis, development, and prognosis of cervical cancer, and presented new potential avenues for cancer therapeutics. [ABSTRACT FROM AUTHOR]

Wilms tumor (WT) is the most common malignant renal neoplasm in children; however, the underlying molecular mechanisms are not well understood. According to the competing endogenous RNA (ceRNA) theory, long non-coding RNAs (lncRNAs) can regulate the expression of target genes by adsorbing microRNAs (miRNAs/miRs). However, the role of lncRNAs in WT has not been fully elucidated. The aim of the present study was to construct a ceRNA network to identify the potential lncRNAs involved in WT. The expression profiles of lncRNAs, miRNAs and mRNAs in 120 WT and six normal tissues were obtained from the Therapeutically Applicable Research to Generate Effective Treatments database. A total of 442 lncRNAs, 214 miRNAs and 4,912 mRNAs were identified as differentially expressed in WT and were enriched in 472 Gene Ontology terms (355 biological processes, 89 cellular components and 29 molecular functions) and 18 Kyoto Encyclopedia of Genes and Genomes pathways. A lncRNA-miRNA-mRNA ceRNA network of WT consisting of with 32 lncRNAs, 14 miRNAs and 158 mRNAs was constructed, based on the bioinformatics analysis of the miR target prediction database and the miRNAcode, miRTarBase and TargetScan databases. Subsequently, three lncRNAs, three miRNAs and 17 mRNAs, which had a significant effect on the overall survival rate of patients with WT, were identified based on the survival analysis. The three lncRNAs were also differentially expressed in the late and early stages of WT and were validated using the GSE66405 dataset obtained from the Gene Expression Omnibus database. In conclusion, the present study generated a specific lncRNA-related ceRNA network of WT, which may provide a novel perspective on the molecular mechanisms underlying the progression and prognosis of the disease. [ABSTRACT FROM AUTHOR]

Methylation is a fundamental regulator of gene transcription. Long non-coding RNA maternally expressed 3 (MEG3) inhibits cell proliferation in various types of cancer. However, the molecular mechanisms of MEG3 methylation in the regulation of multiple myeloma (MM) are unknown. In the present study, MEG3 upregulation was negatively associated with the International Staging System (ISS) status of the bone marrow samples of 39 patients with MM. MEG3 overexpression in an MM cell line resulted in elevated p53 expression. Furthermore, the results of methylation-specific PCR revealed that the abnormal methylation status of the MEG3 promoter region was present in eight of the 39 bone marrow samples collected. Treatment of the MM cell line with the DNA methylation inhibitor 5-Aza-2'-deoxycytidine (5-Aza-CdR) resulted in tumor cell proliferation inhibition, apoptosis induction and G0/G1 cell cycle arrest. Furthermore, 5-Aza-CdR decreased aberrant hypermethylation of the MEG3 promoter and increased the expression of MEG3. However, 5-Aza-CdR exerted no effect on p53 expression. To the best of our knowledge, the present study is the first to report that the demethylation reagent 5-Aza-CdR may serve as a therapeutic agent in MM by upregulating MEG3 expression. However, the mechanism of action was independent of p53 expression. [ABSTRACT FROM AUTHOR]

The human transcriptome is primarily composed of long non-coding RNAs (lncRNAs), which are key regulatory molecules of multiple biological processes. In the present study, the expression profiles of lncRNAs in the peripheral blood and CD4+ T cells of patients with active rheumatoid arthritis (RA) were determined. Based on the expression profiles, 493 lncRNAs and 374 mRNAs were identified to be differentially expressed in the peripheral blood of active RA patients and healthy donors. Further verification of lncRNAs was performed using reverse transcription-quantitative (RT-q) PCR analysis of peripheral blood from 5 healthy donors and 5 patients with active RA and 14 additional differentially expressed genes were identified. CD4+ T cells in peripheral blood from 12 patients with active RA and 8 healthy donors were isolated using magnetic beads and qPCR was used to assess differentially expressed lncRNAs. The results suggested that 7 lncRNAs were upregulated and 2 were downregulated. The results indicated that these 9 lncRNAs may be involved in the pathogenesis of RA. An increased ratio of Th17: T-regulatory (Treg) cells was also observed. It may be hypothesized that LncRNAs serve important roles in the differentiation of CD4+ T cells. Receiver operating characteristic curve analysis suggested that these 9 lncRNAs are of potential clinical diagnostic value for RA. Pearson correlation analysis indicated that the correlation coefficient between Ensembl transcript (ENST)00000569543 and complement C4 was 0.623 (P<0.05), and that between ENST00000420096 and anti-cyclic citrullinated peptide antibody or disease activity evaluation score, the correlation coefficient was 0.662 and 0.605, respectively (P<0.05 for each). In conclusion, the results of the present study suggest a possible role of lncRNAs in the differentiation of CD4+ T cells and the pathogenesis of RA, as well as the potential value as diagnostic biomarkers for active RA. [ABSTRACT FROM AUTHOR]

After the expression level of lncRNA AC023794.4-201 was upregulated in 2 laryngeal squamous cell carcinoma (LSCC) cell lines (AMC-HN-8 and TU-212) and LSCC xenografts, the biological function of lncRNA AC023794.4-201 in LSCC was further investigated using in vitro and in vivo experiments, such as cell function experiments and nude mice transplantation. In our previous study, it was demonstrated that the expression level of the long non-coding RNA (lncRNA) AC023794.4-201 were decreased in laryngeal squamous cell carcinoma, particularly in cases of LSCC with lymphatic metastasis. Moreover, low expression levels of AC023794.4-201 were revealed to be an adverse prognostic factor for patients with LSCC. In the present study, lentiviruses were used to overexpress AC023794.4-201 before a series of cell function assays were performed and a xenograft nude mouse model was constructed, in order to further investigate the functions of AC023794.4-201 in LSCC. AC023794.4-201 inhibited the proliferation and the cloning capacity of LSCC cells compared with the negative control group as indicated by real-time cell analysis and the plate colony formation assay. Flow cytometry and transwell migration assays demonstrated that AC023794.4-201 inhibited the migration, induced cell cycle arrest and increased the apoptotic rate of LSCC cells. The results of the in vivo studies demonstrated that AC023794.4-201 significantly inhibited the growth of LSCC xenografts, and promoted apoptosis. In conclusion, the findings of the present study suggested that AC023794.4-201 may exert tumor-suppressive functions in the progression of LSCC and may serve as a potential prognostic biomarker for LSCC. [ABSTRACT FROM AUTHOR]

The transfer and development of chronic hepatitis B virus (HBV) infection is associated with the T cell immune response, therefore investigating the key regulators of cell immune response is needed to improve chronic HBV treatment. Blood samples from patients with chronic HBV infection were used to confirm the correlation between HBV infection stage and CD160 receptor expression levels in CD8+ T cells, the CD8+ T cells are used to research the mechanism of T cell immune response modulation, moreover, C3H/HeN mice with reduced CD160 expression levels were used to investigate the association between long non-coding (lnc)RNA-CD160 and HBV infection. Long non-coding (lnc)RNA-CD160 and histone-modification enzyme gene histone deacetylase 11 (HDAC11) expression levels were negatively associated with CD160 expression. lncRNA-CD160 can inhibit the secretion of IFN-γ and TNF-α through HDAC11 recruitment and bind to HDAC11 to form a complex on the promoters of IFN-γ and TNF-α. The HDAC11, IFN-γ and TNF-α form a complex and enhance the methylation of H3K9Me1, chromatin changes into the heterochromatin and the transcription of IFN-γ and TNF-α is blocked; moreover, the HDAC11/IFN-γ/TNF-α complex can also inhibit the secretion of IFN-γ and TNF-α in CD160− CD8+ T cells and suppresses the function of CD8+ T cells. Furthermore, small interfering RNA targeting lncRNA-CD160 can block HBV infection progression. lncRNA-CD160 acts as an immune suppressive factor and is expressed at a high level in peripheral blood CD8+ T cells of HBV infected patients. Furthermore, high expression levels of lncRNA-CD160 can contribute to the inhibition of IFN-γ and TNF-α secretion in CD8+ T cells and decrease the immune response of CD8+ T cells. Therefore, lncRNA-CD160 may become a new target for immunotherapy of chronic HBV infection in the future and may provide a new therapeutic strategy for the treatment of HBV infection. [ABSTRACT FROM AUTHOR]

Long non-coding RNAs (lncRNAs) have attracted a lot of attention for their role in the development, progression and prognosis of colorectal cancer (CRC). However, little is known on the clinical significance of the translation regulatory lncRNA 1 (TRERNA1) in CRC. The present study aimed to explore the clinical value of TRERNA1 in patients with CRC. A total of 89 cancer-associated lncRNA genes were analyzed using the RT2 lncRNA PCR array Human Cancer PathwayFinder. Following the PCR array, reverse transcription-quantitative (RT-q)PCR was conducted to identify the differential expression of TRERNA1 between 130 CRC and corresponding non-tumorous adjacent tissues. Additionally, the association between TRERNA1 expression and clinical characteristics was analyzed. Furthermore, TRERNA1 expression was knocked down via small interfering RNAs. The results of the PCR array and RT-qPCR revealed that TRERNA1 expression was significantly upregulated in CRC tissues compared with in adjacent normal tissues. TRERNA1 upregulation was positively associated with distant metastasis, perineural invasion, TNM stage, node metastasis stage and tumor diameter. Multivariate analysis revealed that patients with higher TRERNA1 expression had a shorter overall survival (OS) time and a less favorable prognosis compared with those in the low TRERNA1 expression group. Knockdown of TRERNA1 inhibited invasion and metastasis of CRC cells via regulating Snail expression. In conclusion, TRERNA1 expression was upregulated in CRC tissues. High expression levels of TRERNA1 may be associated with poor OS times, a less favorable prognosis and lymph node metastasis in patients with CRC. TRERNA1 may therefore serve as a useful and novel biomarker for CRC lymph node metastasis and prognosis. [ABSTRACT FROM AUTHOR]

Long non-coding RNA gastric cancer associated transcript 3 (GACAT3), is a newly identified non-coding RNA, which has been found to be involved in the tumorigenesis of gastric cancer. However, the biological function of GACAT3 in liver cancer remains unclear. The present study aimed to determine the expression level and function of GACAT3 in liver cancer. The authors cultured liver cancer cells in vitro and GACAT3 was silenced in the cells. Cell proliferation, apoptosis and migration were determined by MTT assay, flow cytometric analysis and transwell assay, respectively. It was demonstrated that GACAT3 was upregulated in liver cancer tissues. The inhibition of GACAT3 decreased the ability of hepatoma cells to proliferate and migrate, and increased apoptosis of the cells. These findings provide the first evidence, to the best of our knowledge, of the exact role of GACAT3 in liver cancer, suggesting GACAT3 as a potential target for liver cancer therapy in the future. [ABSTRACT FROM AUTHOR]

Long non-coding RNAs (lncRNAs) serve crucial roles in carcinogenesis. Myocardial infarction-associated transcript (MIAT), originally isolated as a candidate gene for myocardial infarction, has been revealed to serve as an oncogene in chronic lymphocytic leukaemias and neuroendocrine prostate cancer. However, little is known about its expression pattern, biological function and underlying mechanism in esophageal cancer. Cell lines of esophageal cancer were used in the current study. The results of the present study revealed that MIAT knockdown decreased cell viability, migration, invasion and cell cycle arrest in the G1 phase. Mechanistic assessment revealed that MIAT interacts with histone methyltransferase mixed-lineage leukemia (MLL). The relative proteins expressions were measured by western blotting assay. MIAT knockdown suppressed cell invasion and migration by regulation MMP-2/9 protein expressions. The results of the current study indicated that MIAT expression was associated with esophageal cancer and may serve as a critical target in the progression and metastasis in esophageal cancer. [ABSTRACT FROM AUTHOR]

Long non-coding RNAs (lncRNAs) are recognized as critical regulators of self-renewal in human cancer stem-like cells (CSCs), which are a subpopulation of cancer cells primarily responsible for the malignant features of cancer. However, most CSC-related lncRNAs remain unidentified. The results of the present study suggested that growth-arrest-specific transcript 5 (GAS5), a tumor suppressor, exhibited increased expression and was associated with malignant features in human colorectal cancer cell HCT116-derived CSCs. Phenotypic analysis indicated that GAS5 knockdown by specific siRNA significantly decreased CSC self-renewal capacity, proliferation and migration. Moreover, GAS5 knockdown sensitized CSCs to the chemotherapeutic agents 5-fluorouracil and doxorubicin by inducing apoptosis detected by Annexin V-FITC/PI double staining. Inhibition of Nodal growth differentiation factor (NODAL) signaling, which has been reported to be protected by GAS5, presented similar chemosensitivity effects to the GAS5 knockdown results. The present study also assessed the effects of GAS5 overexpression on HCT116 cells, and revealed that overexpression of GAS5 sensitized HCT116 cells to chemotherapeutic agents, which is the opposite of the effect observed in CSCs derived from HCT116 cells. Therefore, it was hypothesized that GAS5 may function as a critical factor for maintaining stemness and that it may exert protective effects on CSCs in a NODAL-dependent manner. Collectively, the results of the present study indicate that GAS5 may be a promising therapeutic target for overcoming malignant features and chemoresistance in colorectal cancer cells. [ABSTRACT FROM AUTHOR]

Non-coding RNAs (ncRNAs) regulate numerous genes and influence the progression of various human diseases, including cancer. The role of regulatory ncRNAs implicated in nasopharyngeal carcinoma (NPC), as well as their target genes, remains unclear. The present study aimed to investigate specific long non-coding (lnc)RNAs, circular RNAs (circRNAs) and mRNAs associated with the molecular pathogenesis of NPC, and to predict the underlying target genes of specific lncRNAs and circRNAs. The expression levels of lncRNAs, circRNAs and mRNAs in NPC and chronic nasopharyngitis tissues were detected and analyzed using microarray and bioinformatics techniques. A total of 2.80% lncRNAs (425 upregulated and 431 downregulated) were significantly differentially expressed (DE) between the two tissue types. Additionally, 0.96% circRNAs (18 upregulated and 13 downregulated) were significantly DE, while 2.94% mRNAs (426 upregulated and 341 downregulated) were significantly DE between the two tissue types. In total, 420 NPC-associated nearby encoding genes (196 up- and 224 downregulated) of the DE lncRNAs were identified. Overlap analysis identified 23 DE circRNAs and their corresponding target genes, with 37 microRNAs and 50 mRNAs, from which 14 interaction networks were constructed. Subsequent pathway analysis revealed 221 DE target genes corresponding to 31 key signaling pathways associated with NPC, 14 of which may represent hub genes associated with NPC pathophysiology. Thus, certain lncRNAs, circRNAs and mRNAs are aberrantly expressed in NPC tissues, and partially specific lncRNAs, circRNAs and their target genes may influence the tumorigenesis and progression of NPC. Target prediction and regulatory network identification may help to determine the pathogenic mechanisms of NPC. [ABSTRACT FROM AUTHOR]

Long non-coding RNAs (lncRNAs) have been demonstrated to be aberrantly expressed in several types of tumor, and dysregulated lncRNAs are suggested to play a prognostic role in breast cancer (BC). Estrogen receptor (ER) status is a prognostic factor in patients with ER-negative BC, which is associated with poor prognosis. Thus, the present study developed a prognostic lncRNA signature specifically for ER-negative BC, in order to predict the risk of post-surgery relapse and improve patient prognosis. A gene expression profile containing 1,631 lncRNAs was obtained by investigating and integrating publicly available cohorts of BC. Subsequently, a nine-lncRNA signature was developed and validated in two independent cohorts via the Cox regression model. Using the nine-lncRNA signature, patients in the discovery cohort were divided into high- and low-risk groups, with significantly different disease-free survival [DFS; hazard ratio (HR)=2.718, 95% confidence interval (CI)=2.115-3.494, P<0.0001]. Receiver operating characteristic curve analyses demonstrated that the area under the curve reached 0.908. Similar results were obtained in the two independent cohorts (HR=1.499, 95% CI=0.950-2.365, P=0.04; HR=1.262, 95% CI=1.056-1.510, P=0.01), respectively. Furthermore, the nine lncRNAs were demonstrated to play important roles in the cell invasion and metastasis of different types of tumor. The differentially expressed genes (DEGs) identified between the high- and low-risk groups were consistently high in the discovery and validation cohorts. Functional analysis indicated that these DEGs, as well as genes co-expressed with the nine lncRNAs, were involved in cancer-associated signaling pathways, all of which provide further evidence for the predictive ability of the nine-lncRNA signature. Overall, the present study developed a novel prognostic biomarker for ER-negative BC. [ABSTRACT FROM AUTHOR]

The present study aimed to investigate the involvement of long intergenic non-coding RNA for kinase activation (LINK-A) long non-coding RNA (lncRNA) in osteosarcoma. Plasma levels of LINK-A lncRNA and transforming growth factor β1 (TGF-β1) were measured by reverse transcription-quantitative polymerase chain reaction and ELISA, respectively. Correlation between LINK-A lncRNA and TGF-β1 was analyzed by Pearson correlation coefficient. LINK-A lncRNA and TGF-β1 were upregulated in patients with osteosarcoma compared with healthy controls. LINK-A lncRNA and TGF-β1 were positively correlated in the two groups. LINK-A lncRNA short hairpin RNAs (shRNAs) were transfected into osteosarcoma cell lines and Transwell migration assay, Matrigel invasion assay and flow cytometry were used to evaluate cell migration, invasion and stemness, respectively. Effects of LINK-A lncRNA silencing and overexpression on TGF-β1 expression were analyzed by western blotting. LINK-A lncRNA shRNA silencing inhibited, whereas TGF-β1 treatment promoted cell migration, invasion and stemness. LINK-A lncRNA silencing inhibited TGF-β1 expression, whereas TGF-β1 treatment had no effects on LINK-A lncRNA expression. TGF-β1 reduced the inhibitory effects of LINK-A lncRNA knockdown on cancer cell migration, invasion and stemness. These data indicated that LINK-A lncRNA is upregulated in osteosarcoma and may regulate migration, invasion and stemness of osteosarcoma cells through TGF-β1. [ABSTRACT FROM AUTHOR]

Long non-coding RNAs (lncRNAs) have a number of functions in various cellular processes and are potential prognostic factors for lung adenocarcinoma (LUAD). A gene risk model could provide novel evidence to improve the prediction of overall outcomes and provide more potential biomarkers. The present study aimed improve a previously published method of gene signature construction to make it more robust and accurate. The lncRNA expression profiles from 594 patients with LUAD were obtained from The Cancer Genome Atlas (TCGA) database and samples were divided into high- and low-risk groups based on median risk scores calculated using a prognosis-related risk score formula. Univariate Cox regression, least absolute shrinkage and selection operator algorithm and multivariate Cox regression were performed to construct a gene signature based on the differentially expressed lncRNAs in patients with LUAD. The robustness and accuracy of the present model was assessed using area under the calculated curves (AUC) and Kaplan-Meier (K-M) survival analysis of the high- and low-risk cohorts. Potential biomarkers associated with survival status were then identified using K-M survival analysis and potential biomarker functions were predicted using enrichment analysis of co-expressed mRNAs. The gene signature constructed contained 44 lncRNAs. The AUCs for 3- and 5-year survival with the model were 0.836 and 0.818, respectively, of a time-dependent receiver operator characteristic curve. Moreover, lncRNAs AC124804.1 and MIR34AHG were identified using K-M survival analysis and the potential function of these two lncRNAs was predicted using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes functional enrichment. The present lncRNA model provides novel insight which may improve prediction of prognosis for patients with LUAD and identify potentially novel biomarkers for the diagnosis. [ABSTRACT FROM AUTHOR]

Long intergenic non-coding RNA for kinase activation (LINK-A) has been characterized as an oncogenic long non-coding (lnc)RNA in triple-negative breast cancer and ovarian carcinoma, but its involvement in other malignancies remains elusive. In the present study, it was determined that the plasma levels of LINK-A lncRNA and Rho-associated protein kinase 1 (ROCK1) were significantly increased in patients with pancreatic adenocarcinoma compared with those in healthy controls. The plasma levels of LINK-A lncRNA were positively correlated with the plasma levels of ROCK1 in pancreatic adenocarcinoma patients, but not in healthy controls. Silencing of LINK-A led to inhibition of pancreatic adenocarcinoma cell proliferation, migration and invasion. Simultaneous overexpression of ROCK1 attenuated the inhibitory effect of LINK-A silencing on cancer cell proliferation, migration and invasion. Overexpression of LINK-A lncRNA led to upregulation of ROCK1 expression, while overexpression of ROCK1 had no significant effect on LINK-A lncRNA expression. It may therefore be concluded that LINK-A lncRNA may have a role in pancreatic adenocarcinoma, at least in part, by promoting ROCK1 expression. [ABSTRACT FROM AUTHOR]

Triple-negative breast cancer (TNBC) is a subtype of breast cancer that is characterized by aggressive and metastatic clinical characteristics and generally leads to earlier distant recurrence and poorer prognosis than other molecular subtypes. Accumulating evidence has demonstrated that long non-coding RNAs (lncRNAs) serve a crucial role in a wide variety of biological processes by interacting with microRNAs (miRNAs) as competing endogenous RNAs (ceRNAs) and, thus, affect the expression of target genes in multiple types of cancer. Seven datasets from the Gene Expression Omnibus (GEO) database, including 444 tumor and 88 healthy tissue samples, were utilized to investigate the underlying mechanisms of TNBC and identify prognostic biomarkers. Differentially expressed genes (DEGs) were further validated in The Cancer Genome Atlas database and the associations between their expression levels and clinical information were analyzed to identify prognostic values. A potential lncRNA-miRNA-mRNA ceRNA network was also constructed. Finally, 69 mRNAs from the integrated Gene Expression Omnibus datasets were identified as DEGs using the robust rank aggregation method with |log2FC|>1 and adjusted P<0.01 set as the significance cut-off levels. In addition, 29 lncRNAs, 21 miRNAs and 27 mRNAs were included in the construction of the ceRNA network. The present study elucidated the mechanisms underlying the progression of TNBC and identified novel prognostic biomarkers for TNBC. [ABSTRACT FROM AUTHOR]

Dysregulated expression of long non-coding RNAs has been determined to be important in cancer development; however, their role in tongue squamous cell carcinoma (TSCC) progression and carcinogenesis, to the best of our knowledge, is yet to be elucidated. The present study revealed that long intergenic non-coding RNA 00152 (LINC00152) expression was significantly increased in human TSCC tissues compared with in tissues from matched controls using RT-qPCR. In TSCC cell lines, CAL-27 and SCC-9, LINC00152 was revealed to promote TSCC cell proliferation, enhance cell cycle progression and inhibit cell apoptosis. Additionally, migration and invasion of TSCC cell lines was increased in response to LINC00152 overexpression. Mechanistically, LINC00152 was determined to be localized in the cytoplasm and acted as a microRNA (miR)-193b-3p sponge, and LINC00152 knockdown or miR-193b-3p mimics both inhibited PI3K signaling pathway activation and downstream AKT phosphorylation; therefore, promoting TSCC progression in vitro. Overall, the results of the present study suggested that increased LINC00152 expression in TSCC tissues may act as a sponge of miR-193b-3p to promote cancer progression in vitro. [ABSTRACT FROM AUTHOR]

Acute myocardial infarction (AMI), as the first manifestation of ischemic heart disease, is the most common cause of death in developed countries. A recent study showed that metastasis associated lung adenocarcinoma transcript 1 (MALAT1), a prognostic marker for lung cancer metastasis, could promote myocardial ischemia-reperfusion injury by regulating the levels of microRNA (miR)-145. In order to elucidate the biological function of MALAT1 in the pathogenesis of AMI and to explore the mechanisms underlying its action, an AMI rat model was established by ligation of the left anterior descending coronary artery. Downregulation of MALAT1 by siRNA transfection attenuated heart damage in an AMI model rat. The mouse cardiomyocyte cell line HL-1 was used to show that downregulation of nucleotide binding and oligomerization domain-like receptor C5 (NLRC5) and upregulation of miR-125b-5p were the results of MALAT1 silencing. TargetScan and a dual-luciferase reporter assay indicated that NLRC5 is a direct target of miR-125b-5p. Overexpression of miR-125b-5p significantly reduced hypoxia/reperfusion-induced apoptosis of HL-1 cells, an effect that could be blocked by NLCR5 overexpression. Taken together, these results suggest that MALAT1 reduced the protective effect of miR-125b-5p on injured cells through upregulation of NLCR5. This study highlights the role of MALAT1 in the pathogenesis of AMI and may guide future genetic therapeutic strategies for AMI treatment. [ABSTRACT FROM AUTHOR]

Long non-coding RNAs (lncRNAs) are a subgroup of RNAs able to regulate gene expression at the epigenetic level, and are therefore central to the regulation of numerous biological processes and the progression of multiple cancer types. However, lncRNAs have not been identified to considerably influence overall survival (OS) outcome in numerous different types of cancer. The majority of studies investigating the association between lncRNAs and epigenetic regulation have focused on their altered expression levels in cancerous cells, and few studies have focused on determining the correlation between lncRNAs and OS time. In the present study, comprehensive lncRNA expression analysis was performed on a cohort of patients diagnosed with colon adenocarcinoma (COAD) using the least absolute shrinkage and selection operator method (LASSO). Subsequently, the construction of a prognostic methylation-based predictive system was performed based on the results of LASSO analysis. Functional enrichment analysis of lncRNA co-expression genes was also performed. According to the results of the present study, the classifier was able to significantly predict the prognosis of patients with COAD, and the investigation of the relevant elucidated genes further revealed the mechanism of COAD pathogenesis. [ABSTRACT FROM AUTHOR]

Melanoma is a rare but fatal form of skin cancer and acral lentiginous melanoma (ALM) is one of its most common types. Long non-coding RNA (lncRNA) has emerged as a crucial molecule in the development and progression of human cancers, and several studies have revealed that lncRNAs may be associated with the pathogenesis, progression and metastasis of melanoma. To demonstrate the association between ALM and lncRNAs, microarray analysis was performed in tumor and adjacent non-tumor tissues. A total of 4,488 lncRNAs and 3,913 mRNAs were identified to be differentially expressed in these samples. Among them, 2,211 and 2,277 lncRNAs were upregulated and downregulated in the ALM samples compared with adjacent tissues, respectively. In addition, 1,191 and 2,722 mRNAs were upregulated and downregulated, respectively. Additionally, five randomly selected lncRNAs (fold-change >2; P<0.05) were validated by reverse transcription-quantitative PCR. An lncRNA and mRNA co-expression network and competing endogenous network analysis were also constructed. In summary, the results of the present study may reveal a novel mechanism associated with the pathogenesis and malignant biological processes of ALM and indicate that lncRNAs may serve as potential targets for the treatment of ALM. [ABSTRACT FROM AUTHOR]

Breast cancer (BC) is one of the most common fatal cancers. Recent studies have identified the vital role of long non-coding RNAs (lncRNAs) in the development and progression of BC. In this investigation, lncRNA TTN-AS1 was studied to identify its function in the metastasis of BC. TTN-AS1 expression of tissues was detected by real-time quantitative polymerase chain reaction (RT-qPCR) in 56 BC patients. Wound healing assay and transwell assay were used to observe the biological behavior changes of BC cells through gain or loss of TTN-AS1. In addition, luciferase assays and RNA immunoprecipitation (RIP) assay were performed to discover the potential targets of TTN-AS1 in BC cells. TTN-AS1 expression level in BC samples was higher than that of adjacent tissue. Besides, the ability of cell migration and invasion of BC cells was inhibited after TTN-AS1 was silenced, while cell migration and cell invasion of BC cells were promoted after TTN-AS1 was overexpressed. In addition, miR-140-5p was upregulated after silencing of TTN-AS1 in BC cells, while miR-140-5p was downregulated after overexpression of TTN-AS1 in BC cells. Furthermore, luciferase assays and RIP assay showed that miR-140-5p was a direct target of TTN-AS1 in BC. Our study uncovered a new oncogene in BC and suggests that TTN-AS1 enhances BC cell migration and invasion via sponging miR-140-5p, which provides a novel therapeutic target for BC patients. [ABSTRACT FROM AUTHOR]

Breast cancer (BC) is one of the most dangerous malignant diseases among women. A growing amount of evidence has suggested that long non-coding RNAs participate in the development and progression of BC and may potentially serve as therapeutic targets or prognostic markers for the disease. A previous study demonstrated that long intergenic non-protein coding RNA 01140 (LINC01140) was prominently correlated with overall survival in patients with gastric cancer. However, the function of LINC01140 in BC has not yet been elucidated. Therefore, the present study aimed to investigate the roles and molecular mechanisms underlying LINC01140 in BC. LINC01140 expression in 1,085 breast cancer patients and 291 healthy subjects was analyzed from the Gene Expression Profiling Interactive Analysis website. The association between LINC01140 expression and T stages, LINC01140-related biological pathways, and the correlation between LINC01140 expression genes were also analyzed in 825 patients with BC through the cBioPortal database. The present study demonstrated that LINC01140 expression was significantly decreased in the tumor samples compared with normal samples in patients with BC (P<0.05). The present study revealed that LINC01140 expression was significantly decreased in the T4 stage compared with T1, T2 or T3 stage (P<0.01). In addition, high expression levels of LINC01140 predicts longer relapse-free survival probability in patients with BC. It was also observed that LINC01140 participates in a variety of biological pathways, particularly in the epithelial-to-mesenchymal transition. The co-expression relationship between the LINC01140 and an abundance of genes in samples from the BC study was investigated. These genes, such as chordin like 1 and bone morphogenic protein 6, participate in the development and progression of tumor growth and bone metastasis. Finally, the present study observed the interaction between microRNA (miR)-200b and miR-200c with LINC011440. The results from the present study indicated that higher expression of LINC01140 was beneficial for patients with BC. LINC01140 may be a potential biomarker for the prognosis of patients with BC. The role of LINC01140 in BC needs to be further evaluated. [ABSTRACT FROM AUTHOR]