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Background: Periodontitis is the most common oral disease and is closely related to immune infiltration in the periodontal microenvironment and its poor prognosis is related to the complex immune response. The progression of periodontitis is closely related to necroptosis, but there is still no systematic study of long non-coding RNA (lncRNA) associated with necroptosis for diagnosis and treatment of periodontitis. Material and methods: Transcriptome data and clinical data of periodontitis and healthy populations were obtained from the Gene Expression Omnibus (GEO) database, and necroptosis-related genes were obtained from previously published literature. FactoMineR package in R was used to perform principal component analysis (PCA) for obtaining the necroptosis-related lncRNAs. The core necroptosis-related lncRNAs were screened by the Linear Models for Microarray Data (limma) package in R, PCA principal component analysis and lasso algorithm. These lncRNAs were then used to construct a classifier for periodontitis with logistic regression. The receiver operating characteristic (ROC) curve was used to evaluate the sensitivity and specificity of the model. The CIBERSORT method and ssGSEA algorithm were used to estimate the immune infiltration and immune pathway activation of periodontitis. Spearman's correlation analysis was used to further verify the correlation between core genes and periodontitis immune microenvironment. The expression level of core genes in human periodontal ligament cells (hPDLCs) was detected by RT-qPCR. Results: A total of 10 core necroptosis-related lncRNAs (10-lncRNAs) were identified, including EPB41L4A-AS1, FAM30A, LINC01004, MALAT1, MIAT, OSER1-DT, PCOLCE-AS1, RNF144A-AS1, CARMN, and LINC00582. The classifier for periodontitis was successfully constructed. The Area Under the Curve (AUC) was 0.952, which suggested that the model had good predictive performance. The correlation analysis of 10-lncRNAs and periodontitis immune microenvironment showed that 10-lncRNAs had an impact on the immune infiltration of periodontitis. Notably, the RT-qPCR results showed that the expression level of the 10-lncRNAs obtained was consistent with the chip analysis results. Conclusions: The 10-lncRNAs identified from the GEO dataset had a significant impact on the immune infiltration of periodontitis and the classifier based on 10-lncRNAs had good detection efficiency for periodontitis, which provided a new target for diagnosis and treatment of periodontitis. [ABSTRACT FROM AUTHOR]

HML6-c14, a long terminal repeat (LTR)-type retrotransposon identified by expressed sequence tag (EST) database screening, was found to undergo RNA processing resembling that of placental tissue by in vitro expression analysis. Previous in situ hybridization studies using normal placental tissue showed that the transcript remained in the nucleus. However, among the transcripts forcedly expressed in cultured cells, the transcript that retained the 3.3 kb intron was observed in the nucleus, and a part of the spliced transcript was observed outside the nucleus. To verify whether this cytoplasmic transcript could be translated, we examined the coding potential of the open reading frame (ORF), consisting of 109 codons on the spliced transcript, along with two other putative ORFs detected in the intronic region. As a result, none of the ORF-derived products could be detected by Western blotting as fusion proteins tagged with the FLAG epitope, suggesting that HML6-c14 belongs to a group of long non-coding RNA (lncRNA) genes. Promoter analysis of the upstream 6.4 kb genomic region also suggested that the 5′-LTR itself potentially retains high promoter activity. Despite losing the ability to produce functional proteins, HML6-c14 continues to retain its transcriptional ability while converting to an lncRNA gene, which is an interesting subject for future research. [ABSTRACT FROM AUTHOR]

Simple Summary: The intrinsic radioresistance of cancer cells is a major barrier to effective radiotherapy for NSCLC. The long non-coding RNA, endogenous bornavirus-like nucleoprotein 3 (LNC EBLN3P), was initially discovered to exhibit upregulation in NSCLC and promote the progression of NSCLC. The aim of this study was to elucidate the correlation between elevated expression levels of LNC EBLN3P and radioresistance in NSCLC cells, as well as to investigate the underlying molecular mechanism. We confirmed that the inhibition of LNC EBLN3P can enhance the production of reactive oxygen species (ROS) and trigger mitochondrial impairment in NSCLC cells, thereby mitigating the radioresistance of NSCLC cells. Therefore, the inhibition of LNC EBLN3P presents a promising approach for the development of novel radiosensitizers. Lung cancer remains the leading cause of cancer-related deaths in both women and men, claiming millions of lives worldwide. Radiotherapy is an effective modality for treating early-stage lung cancer; however, it cannot completely eradicate certain tumor cells due to their radioresistance. Radioresistance is commonly observed in conventionally fractionated radiotherapy, which can lead to treatment failure, metastasis, cancer recurrence, and poor prognosis for cancer patients. Identifying the underlying molecular mechanisms of radioresistance in lung cancer can promote the development of effective radiosensitizers, thereby improving patients' life expectancy and curability. In this study, we identified LNC EBLN3P as a regulator of lung cancer cell proliferation and radiosensitivity. The repression of LNC EBLN3P could increase ROS production and mitochondrial injury in NSCLC cells. In addition, knocking down LNC EBLN3P increased the binding of Nrf2 to Keap1, resulting in enhanced Nrf2 degradation, decreased translocation of Nrf2 to the nucleus, reduced expression of antioxidant protein HO-1, weakened cellular antioxidant capacity, and increased radiosensitivity of NSCLC cells. These findings suggest that targeting LNC EBLN3P could be a promising strategy for developing novel radiosensitizers in the context of conventional radiotherapy for NSCLC. [ABSTRACT FROM AUTHOR]

This study aims to discuss the role of exosomes KCNQ10T1 derived from bone marrow mesenchymal stem cells (BMMSCs) in sepsis and to further investigate its potential molecular mechanisms. Exosomes extracted from BMMSCs are identified by transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA), and western blot. Fluorescence labeling is applied to detect the internalization of exosomes in receptors. The proliferation ability, migration ability, and invasion ability of HUVECs are determined by CCK-8, EdU, wound healing, and Transwell. The levels of inflammatory cytokines in sepsis cells are quantitatively detected by ELISA. Kaplan–Meier survival curve is used to describe the overall survival. RT-qPCR is used to detect mRNA expression of related genes. Bioinformatics analysis is performed to search the downstream target of KCNQ1OT1 and miR-154-3p and the interaction is verified by luciferase reporter assay. Exosomes derived from BMMSCs alleviated the toxicity in sepsis cell models and animal models. In mice with septic cell models, exosomal KCNQ10T1 was down-regulated and associated with lower survival. Overexpression of KCNQ10T1 inhibited the proliferation and metastasis of LPS-induced HUVECs. Further research illustrated that miR-154-3p was the downstream target gene of KCNQ1OT1 and RNF19A was the downstream target gene of miR-154-3p. Importantly, functional research findings indicated that KCNQ1OT1 regulated sepsis progression by targeting miR-154-3p/RNF19A axis. Our study demonstrates that the exosomal KCNQ1OT1 suppresses sepsis via mediating miR-154-3p/RNF19A, which provides a latent target for sepsis treatment. [ABSTRACT FROM AUTHOR]

Knee osteoarthritis (KOA) is a chronic joint bone disease characterized by inflammatory destruction and hyperplasia of bone. Its main clinical symptoms are joint mobility difficulties and pain, severe cases can lead to limb paralysis, which poses major pressure to the quality of life and mental health of patients, but also brings serious economic burden to society. The occurrence and development of KOA is influenced by many factors, including systemic factors and local factors. The joint biomechanical changes caused by aging, trauma and obesity, abnormal bone metabolism caused by metabolic syndrome, the effects of cytokines and related enzymes, genetic and biochemical abnormalities caused by plasma adiponectin, etc. all directly or indirectly lead to the occurrence of KOA. However, there is little literature that systematically and comprehensively integrates macro‐ and microscopic KOA pathogenesis. Therefore, it is necessary to comprehensively and systematically summarize the pathogenesis of KOA in order to provide a better theoretical basis for clinical treatment. [ABSTRACT FROM AUTHOR]

Multiple sclerosis（ MS） is an inflammatory demyelinating disease of the central nervous system, specific pathogenesis of which is still unclear. Long chain non-coding RNA（lncRNA） without protein coding function, which were found in playing important functions in many diseases. In recent years, some patients with MS and animal model of experimental autoimmune encephalomyelitis （EAE） were discovered that expressed a large number of abnormal lncRNA. In this paper, lncRNA involved in MS and EAE models are summarized briefly, focusing on the current research status of lncRNA in the pathogenesis of MS. [ABSTRACT FROM AUTHOR]

DNA methylation (5mC) and N6-methyladenosine (m6A) are two important epigenetics regulators, which have a profound impact on plant growth development. Phyllostachys edulis (P. edulis) is one of the fastest spreading plants due to its well-developed root system. However, the association between 5mC and m6A has seldom been reported in P. edulis. In particular, the connection between m6A and several post-transcriptional regulators remains uncharacterized in P. edulis. Here, our morphological and electron microscope observations showed the phenotype of increased lateral root under RNA methylation inhibitor (DZnepA) and DNA methylation inhibitor (5-azaC) treatment. RNA epitranscriptome based on Nanopore direct RNA sequencing revealed that DZnepA treatment exhibits significantly decreased m6A level in the 3′-untranslated region (3′-UTR), which was accompanied by increased gene expression, full-length ratio, higher proximal poly(A) site usage and shorter poly(A) tail length. DNA methylation levels of CG and CHG were reduced in both coding sequencing and transposable element upon 5-azaC treatment. Cell wall synthesis was impaired under methylation inhibition. In particular, differentially expressed genes showed a high percentage of overlap between DZnepA and 5-azaC treatment, which suggested a potential correlation between two methylations. This study provides preliminary information for a better understanding of the link between m6A and 5mC in root development of moso bamboo. [ABSTRACT FROM AUTHOR]

Pancreatic ductal adenocarcinoma (PDAC) is one of humans' most common and fatal neoplasms. Nowadays, a number of PDAC studies are being conducted in two different fields: non-coding RNA (especially microRNA and long non-coding RNA) and microbiota. It has been recently discovered that not only does miRNA affect particular bacteria in the gut microbiome that can promote carcinogenesis in the pancreas, but the microbiome also has a visible impact on the miRNA. This suggests that it is possible to use the combined impact of the microbiome and noncoding RNA to suppress the development of PDAC. Nevertheless, insufficient research has focused on bounding both approaches to the diagnosis, treatment, and prevention of pancreatic ductal adenocarcinoma. In this article, we summarize the recent literature on the molecular basis of carcinogenesis in the pancreas, the two-sided impact of particular types of non-coding RNA and the pancreatic cancer microbiome, and possible medical implications of the discovered phenomenon. [ABSTRACT FROM AUTHOR]

Imprinted genes play diverse roles in mammalian development, homeostasis, and disease. Most imprinted chromosomal domains express one or more long non-coding RNAs (lncRNAs). Several of these lncRNAs are strictly nuclear and their mono-allelic expression controls in cis the expression of protein-coding genes, often developmentally regulated. Some imprinted lncRNAs act in trans as well, controlling target gene expression elsewhere in the genome. The regulation of imprinted gene expression—including that of imprinted lncRNAs—is susceptible to stochastic and environmentally triggered epigenetic changes in the early embryo. These aberrant changes persist during subsequent development and have long-term phenotypic consequences. This review focuses on the expression and the cis- and trans-regulatory roles of imprinted lncRNAs and describes human disease syndromes associated with their perturbed expression. [ABSTRACT FROM AUTHOR]

Recent publications confirmed that long non-coding RNAs (lncRNAs) perform an essential function in gene-specific transcription regulation. Nevertheless, despite its important role, lncRNA has not yet been described in equine sarcoids, the skin neoplasia of horses. Therefore, the aim of this study is to deepen the knowledge about lncRNA expression in the pathogenesis of equine sarcoids and provide new insight into the regulatory function of lncRNA in the bovine papillomavirus–dependent neoplasia of horse dermal tissues. RNA sequencing (RNA-seq) data from 12 equine sarcoid samples and the corresponding controls were reanalyzed in this study. A total of 3396 differentially expressed (DE) lncRNAs and 128 DElncRNA-DE genes (DEGs) pairs were identified. Differentially expressed lncRNAs predicted target genes were enriched in pathways associated with inter alia the extracellular matrix disassembly and cancer pathways. Furthermore, methylation data from the same samples were integrated into the analysis, and 12 DElncRNAs were described as potentially disturbed by aberrant methylation. In conclusion, this study presents novel data about lncRNA’s role in the pathogenesis of equine sarcoids. [ABSTRACT FROM AUTHOR]

The prevalence of osteoporosis (OP) has been continuously increasing in recent years and has gradually become a major public health problem in China. Chronic pain, limited mobility, prolonged bed rest and physical deformity caused by vertebral fractures, hip fractures and wrist fractures caused by osteoporosis have seriously affected the quality of life of patients. This paper intends to provide a new idea for the diagnosis, treatment and prevention of osteoporosis by summarizing the effects of long non-coding RNA (lncRNA)-regulated bone metabolism-related factors on osteoporosis. Some studies have demonstrated that lncRNAs can participate in bone metabolism through various signaling pathways, but the current research on lncRNA-regulated factors is not comprehensive enough, and their specific mechanisms of action and functions need to be further explored, and their application as targeted therapies in clinical settings is also challenging. [ABSTRACT FROM AUTHOR]

Objective To discuss the effect of long non-coding RNA (lncRNA) gastric cancer related transcript 2 (GACAT2) gene on the proliferation and stemness of the lung cancer A549 and H1299 cells, and to clarify the effect of lncRNA GACAT2 gene on the occurrence and development of lung cancer. Methods The full-length sequence of lncRNA GACAT2 gene was amplified by real-time fluorescence quantitative PCR (RT-qPCR) method, and was cloned into the pc3.1 (+) eukaryotic expression vector. The construction of GACAT2 over-expression vector was confirmed by bacterial liquid PCR method and gene sequencing. The pc3.1-GACAT2 over-expression plasmid and control plasmid pc3.1 were separately transfected into the human lung cancer A549 and H1299 cells. The A549 and H1299 cells with stable over-expression of GACAT2 were established by G418 screening, and the cells were divided into blank vector group (transfected with pc3.1 empty vector) and pc3.1-GACAT2 group (transfected with pc3.1-GACAT2 recombinant plasmid). RT-qPCR method was used to detect the expression levels of GACAT2 mRNA in the A549 and H1299 cells in two groups; CCK-8 assay was used to detect the proliferation activities of the cells in two groups; cell clone formation assay was used to detect the clone formation numbers of the cells in two groups; stem cell sphere formation experiment was used to detect the sphere formation numbers of the A549 and H1299 cells in two groups. Results The eukaryotic over-expression vector of GACAT2 was successfully constructed. Compared with blank vector group, the expression levels of GACAT2 mRNA in the A549 and H1299 cells in pc3.1-GACAT2 group were increased (P<0.05 or P<0.01), the cell proliferation activities were decreased (P<0.05 or P<0.01), the clone formation numbers were decreased (P<0.05 or P<0.01), and the sphere formation numbers were decreased (P<0.05 or P<0.01). Conclusion Over-expression of human lncRNA GACAT2 gene can inhibit the proliferation and stemness of the lung cancer A549 and H1299 cells. [ABSTRACT FROM AUTHOR]

Introduction: Diabetic kidney disease (DKD) has become the leading cause of end-stage kidney disease (ESKD) in most countries. Recently, long noncoding RNA XIST has been found involved in the development of DKD. Methods: A total of 1184 hospitalized patients with diabetes were included and divided into four groups based on their estimated glomerular filtration rate (eGFR) and urinary albumin to creatinine ratio (UACR): normal control group (nDKD), DKD with normoalbuminuric and reduced eGFR (NA-DKD), DKD with albuminuria but without reduced eGFR (A-DKD), and DKD with albuminuria and reduced eGFR (Mixed), and then their clinical characteristics were analyzed. Peripheral blood mononuclear cells (PBMCs) of patients with DKD were isolated, and lncRNA XIST expression was detected by real-time quantitative PCR. Results: The prevalence of DKD in hospitalized patients with diabetes mellutus (DM) was 39.9%, and the prevalence of albuminuria and decreased eGFR was 36.6% and 16.2%, respectively. NA-DKD, A-DKD, and Mixed groups accounted for 23.7%, 3.3%, and 12.9%, respectively. Women with DKD had considerably lower levels of lncRNA XIST expression in their PBMCs compared to nDKD. There was a significant correlation between eGFR level and lncRNA XIST expression (R = 0.390, P = 0.036) as well as a negative correlation between HbA1c and lncRNA XIST expression (R = − 0.425, P = 0.027) in female patients with DKD. Conclusions: Our study revealed that 39.9% of DM inpatients who were admitted to the hospital had DKD. Importantly, lncRNA XIST expression in PBMCs of female patients with DKD was significantly correlated with eGFR and HbA1c. [ABSTRACT FROM AUTHOR]

Background: Long non‐coding RNA BRAF‐activated non‐protein coding RNA plays bidirectional roles in human cancers. However, function and molecular mechanism of BRAF‐activated non‐protein coding RNA in oral squamous cell carcinoma still need to clarify further. Methods: Long non‐coding RNA microarray assay, in situ hybridization staining, clinicopathological data analysis were performed to investigate expression pattern of BRAF‐activated non‐protein coding RNA in oral squamous cell carcinoma tissue samples. Constructing ectopically expressed BRAF‐activated non‐protein coding RNA in oral squamous cell carcinoma cells via plasmids or siRNAs, then changeable abilities of proliferation and motility of these cells were observed in vitro and in vivo. RNA‐protein pulldown, RNA immunoprecipitation, and bioinformatics analyses were performed to explore potential pathways involved in BRAF‐activated non‐protein coding RNA‐based regulation of malignant progression in oral squamous cell carcinoma. Results: BRAF‐activated non‐protein coding RNA was identified upregulated in oral squamous cell carcinoma tissue and correlated with nodal metastasis and clinical severity of patients. Overexpressed BRAF‐activated non‐protein coding RNA increased percentage of 5‐ethynyl‐2′‐deoxyuridine‐positive cells, viability, migration, and invasion rates of oral squamous cell carcinoma cells, while silenced BRAF‐activated non‐protein coding RNA could observe weakened effects in vitro. Xenograft tumor formed by BRAF‐activated non‐protein coding RNA‐overexpressed cells had bigger volume, faster growth rates, higher weight, and more Ki67+ cells. Pulmonary metastasis induced by BRAF‐activated non‐protein coding RNA‐silenced cells had fewer colony nodes, Ki67+ cells, and CD31+ blood vessels. Furthermore, BRAF‐activated non‐protein coding RNA was mainly localized in nucleus of oral squamous cell carcinoma cells and bound Ras‐associated binding 1A. Silencing Ras‐associated binding 1A could damage mobile ability and phosphorylation levels of nuclear factor‐κB in oral squamous cell carcinoma cells induced by overexpressing BRAF‐activated non‐protein coding RNA. Opposite trend was also observed. Conclusion: Acting as a promoter in oral squamous cell carcinoma metastasis, BRAF‐activated non‐protein coding RNA promotes oral squamous cell carcinoma cells proliferation and motility by regulating the BRAF‐activated non‐protein coding RNA/Ras‐associated binding 1A complex, which activates nuclear factor‐κB signaling pathway. [ABSTRACT FROM AUTHOR]

Long non-coding RNAs (lncRNAs) play critical role in the pathogenesis of neurodegenerative diseases. Human plasma contains lncRNAs that are present in the blood, and their disease-specific profile has been considered a potential biomarker in some diseases. This study reports screening of the plasma levels of lncRNAs between Alzheimer disease(AD) (n = 45) and matched healthy controls (n = 45). The plasma samples of 5 AD patients and 5 matched healthy controls were randomly selected for expression levels of lncRNAs using the TruSeq RNA Sample Prep Kit (Illumina). The receiver operating characteristic (ROC) curve and area under the curve (AUC) were used to study the potential of lncRNAs as biomarkers. The differential expression profiles of plasma showed that 514 lncRNAs were upregulated, whereas 499 lncRNAs were downregulated.We found that the lncRNAs AL133415.1, AC020916.1, ENST00000654948, ASMTL-AS, AC005730.3, and AP001363.1 levels in the plasma of the AD patients were significantly lower compared to the control group (p1 = 0.0006, p2 < 0.001, p3 < 0.001, p4 = 0.039, p5 = 0.006, p6 < 0.001, respectively). ROC curve analysis revealed that the AUC of AL133415.1 was 0.635 (95% CI]: 0.507–0.763, p = 0.036), the AUC of ASMTL-AS1 was 0.658 (95% CI: 0.513–0.785, p = 0.015), the AUC of AC005730.3 was 0.627 (95%CI: 0.498–0.756, p = 0.049), and the AUC of AP001363.1 was 0.708 (95%CI: 0.595–0.822, p = 0.001). This study indicated that the plasma levels of the lncRNAs ASMTL-AS1, AP001363.1, AC005730.3, and AL133415.1 might be considered potential biomarkers for AD in the Chinese Population. [ABSTRACT FROM AUTHOR]

COVID-19, a disease caused by the SARS-CoV-2 virus, poses significant threats to the respiratory system and other vital organs. Long non-coding RNAs have emerged as influential epigenetic regulators and promising biomarkers in respiratory ailments. The objective of this study was to identify candidate lncRNAs in SARS-CoV-2-positive individuals compared to SARS-CoV-2-negative individuals and investigate their potential association with ARDS-CoV-2 (acute respiratory distress syndrome). Employing qRT-PCR, we meticulously examined the expression profiles of a panel comprising 84 inflammation-related lncRNAs in individuals presenting upper respiratory infection symptoms, categorizing them into those testing negative or positive for SARS-CoV-2. Notably, first-phase PSD individuals exhibited significantly elevated levels of AC000120.7 and SENP3-EIF4A1. In addition, we measured the expression of two lncRNAs, AC000120.7 and SENP3-EIF4A1, in patients with ARDS unrelated to SARS-CoV-2 (n = 5) and patients with ARDS induced by SARS-CoV-2 (ARDS-CoV-2, n = 10), and interestingly, expression was also higher among patients with ARDS. Intriguingly, our interaction pathway analysis unveiled potential interactions between lncRNA AC000120.7, various microRNAs, and genes associated with inflammation. This study found higher expression levels of lncRNAs AC000120.7 and SENP3-EIF4A1 in the context of infection-positive COVID-19, particularly within the complex landscape of ARDS. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Modern Laboratory Medicine is the property of Journal of Modern Laboratory Medicine Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Modern Laboratory Medicine is the property of Journal of Modern Laboratory Medicine Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Sichuan University (Medical Science Edition) is the property of Editorial Board of Journal of Sichuan University (Medical Sciences) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of China Medical University is the property of Journal of China Medical University Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Across the world, oral cancer is a prevalent tumor. Over the years, both its mortality and incidence have grown. Oral cancer metastasis is a complex process involving cell invasion, migration, proliferation, and egress from cancer tissue either by lymphatic vessels or blood vessels. MicroRNAs (miRNAs) are essential short non-coding RNAs, which can act either as tumor suppressors or as oncogenes to control cancer development. Cancer metastasis is a multi-step process, in which miRNAs can inhibit or stimulate metastasis at all stages, including epithelial-mesenchymal transition, migration, invasion, and colonization, by targeting critical genes in these pathways. On the other hand, long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs), two different types of non-coding RNAs, can regulate cancer metastasis by affecting gene expression through cross-talk with miRNAs. We reviewed the scientific literature (Google Scholar, Scopus, and PubMed) for the period 2000–2023 to find reports concerning miRNAs and lncRNA/circRNA-miRNA-mRNA networks, which control the spread of oral cancer cells by affecting invasion, migration, and metastasis. According to these reports, miRNAs are involved in the regulation of metastasis pathways either by directly or indirectly targeting genes associated with metastasis. Moreover, circRNAs and lncRNAs can induce or suppress oral cancer metastasis by acting as competing endogenous RNAs to inhibit the effect of miRNA suppression on specific mRNAs. Overall, non-coding RNAs (especially miRNAs) could help to create innovative therapeutic methods for the control of oral cancer metastases. [ABSTRACT FROM AUTHOR]

Brown planthopper (Nilaparvata lugens Stål, BPH) is one of the most destructive pests of rice. Non-coding RNA plays an important regulatory role in various biological processes. However, comprehensive identification and characterization of long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) in BPH-infested rice have not been performed. Here, we performed a genome-wide analysis of lncRNAs and circRNAs in BPH6-transgenic (resistant, BPH6G) and Nipponbare (susceptible, NIP) rice plants before and after BPH feeding (early and late stage) via deep RNA-sequencing. A total of 310 lncRNAs and 129 circRNAs were found to be differentially expressed. To reveal the different responses of resistant and susceptible rice to BPH herbivory, the potential functions of these lncRNAs and circRNAs as competitive endogenous RNAs (ceRNAs) were predicted and investigated using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses. Dual-luciferase reporter assays revealed that miR1846c and miR530 were targeted by the lncRNAs XLOC_042442 and XLOC_028297, respectively. In responsive to BPH infestation, 39 lncRNAs and 21 circRNAs were predicted to combine with 133 common miRNAs and compete for miRNA binding sites with 834 mRNAs. These mRNAs predictably participated in cell wall organization or biogenesis, developmental growth, single-organism cellular process, and the response to stress. This study comprehensively identified and characterized lncRNAs and circRNAs, and integrated their potential ceRNA functions, to reveal the rice BPHresistance network. These results lay a foundation for further study on the functions of lncRNAs and circRNAs in the rice-BPH interaction, and enriched our understanding of the BPH-resistance response in rice. [ABSTRACT FROM AUTHOR]

Long non-coding RNAs have recently attracted considerable attention due to their aberrant expression in human diseases. LncMIR31HG is a novel lncRNA that is abnormally expressed in multiple diseases and implicated in various stages of disease progression. A large proportion of recent studies have indicated that MIR31HG has biological functions by triggering various signalling pathways in the pathogenesis of human diseases, especially cancers. More importantly, the abnormal expression of MIR31HG makes it a potential biomarker in diagnosis and prognosis, as well as a promising target for treatments. This review aims to systematically summarize the gene polymorphism, expression profiles, biological roles, underlying mechanisms, and clinical applications of MIR31HG in human diseases. [ABSTRACT FROM AUTHOR]

Background: Hepatocellular carcinoma (HCC) is the deadliest malignancy. Long non-coding RNAs (lncRNAs) are involved in the development of multiple human malignancies. This study aimed to establish a reliable signature and identify novel biomarkers for HCC patients. Methods: Differentially expressed lncRNAs (DElncRNAs) were identified from Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases. Univariate, LASSO, and multivariate Cox regression analyses were applied to screen the prognostic lncRNAs and establish a prognostic model. Receiver operating characteristic (ROC) curves and Kaplan-Meier analyses were conducted to validate the prognostic value of this model. The association between lncRNAs and differential m6A genes was analyzed by Spearman's analysis. A series of bioinformatic and in vitro experiments were applied to explore the function of hub lncRNA. Results: A total of 32 DElncRNAs were identified, and 12 DElncRNAs were associated with the prognosis of HCC patients. A prognostic signature comprising six prognostic lncRNAs (LINC02428, LINC02163, AC008549.1, AC115619.1, CASC9, and LINC02362) was constructed, and the model exhibited an excellent capacity for prognosis prediction. Furthermore, 12 differential m6A regulators were identified, and RBMX was found to be correlated negatively with the hub lncRNA AC115619.1. The expression level of AC115619.1 was lower in HCC tissues than that in normal tissues and was significantly related to clinicopathologic features, survival rate, and drug sensitivity. Overexpression of AC115619.1 notably inhibited the proliferation, migration, and invasion of HCC cells. Conclusion: This study provided a promising prognostic signature for HCC patients and identified AC115619.1 as a novel biomarker, which plays an essential role in regulating the progression of HCC. [ABSTRACT FROM AUTHOR]

Primary sensory neurons regulate inflammatory processes in innervated regions through neuro-immune communication. However, how their immunemodulating functions are regulated in concert remains largely unknown. Here, we show that Neat1 long non-coding RNA (lncRNA) organizes the proinflammatory gene expressions in the dorsal root ganglion (DRG) in chronic intractable neuropathic pain in rats. Neat1 was abundantly expressed in the DRG and was upregulated after peripheral nerve injury. Neat1 overexpression in primary sensory neurons caused mechanical and thermal hypersensitivity, whereas its knockdown alleviated neuropathic pain. Bioinformatics analysis of comprehensive transcriptome changes indicated the inflammatory response was the most relevant function of genes upregulated through Neat1. Consistent with this, upregulation of proinflammatory genes in the DRG following nerve injury was suppressed by Neat1 knockdown. Expression changes of these proinflammatory genes were regulated through Neat1-mRNA interaction-dependent and -independent mechanisms. Notably, Neat1 increased proinflammatory genes by stabilizing its interacting mRNAs in neuropathic pain. Finally, Neat1 in primary sensory neurons contributed to spinal inflammatory processes that mediated peripheral neuropathic pain. These findings demonstrate that Neat1 lncRNA is a key regulator of neuroimmune communication in neuropathic pain. [ABSTRACT FROM AUTHOR]

Long non-coding RNAs (lncRNAs), which are RNA transcripts exceeding 200 nucleotides were believed to lack any protein-coding capacity. But advancements in -omics technology have revealed that some lncRNAs have small open reading frames (sORFs) that can be translated by ribosomes to encode peptides, some of which have important biological functions. These encoded peptides subserve important biological functions by interacting with their targets to modulate transcriptional or signalling axes, thereby enhancing or suppressing cardiovascular disease (CVD) occurrence and progression. In this review, we summarize what is known about the research strategy of lncRNA-encoded peptides, mainly comprising predictive websites/tools and experimental methods that have been widely used for prediction, identification, and validation. More importantly, we have compiled a list of lncRNA- encoded peptides, with a focus on those that play significant roles in cardiovascular physiology and pathology, including ENSRNOT (RNO)-sORF6/RNO-sORF7/RNO-sORF8, dwarf open reading frame (DOWRF), myoregulin (NLN), etc. Additionally, we have outlined the functions and mechanisms of these peptides in cardiovascular physiology and pathology, such as cardiomyocyte hypertrophy, myocardial contraction, myocardial infarction, and vascular remodelling. Finally, an overview of the existing challenges and potential future developments in the realm of lncRNA-encoded peptides was provided, with consideration given to prospective avenues for further research. Given that many lncRNA-encoded peptides have not been functionally annotated yet, their application in CVD diagnosis and treatment still requires further research. [ABSTRACT FROM AUTHOR]

Simple Summary: Triple-negative breast cancer accounts for 15–20% of breast tumors. It is a very aggressive and heterogeneous disease characterized by the absence of druggable molecular targets. In that context, understanding the role of non-coding RNAs and their implication in tumorigenesis could represent an opportunity for the development of new therapeutic strategies, as well as for the identification of reliable prognostic biomarkers. Recurrence and development of drugs-resistance represents the most challenging aspects in triple-negative breast cancer. Non-coding RNAs' unique characteristics make them reliable biomarkers for monitoring cancer treatment, potentially able to identify recurrence or chemoresistance. Breast cancer is one of the most frequent causes of cancer death among women worldwide. In particular, triple-negative breast cancer (TNBC) represents the most aggressive breast cancer subtype because it is characterized by the absence of molecular targets, thus making it an orphan type of malignancy. The discovery of new molecular druggable targets is mandatory to improve treatment success. In that context, non-coding RNAs represent an opportunity for modulation of cancer. They are RNA molecules with apparently no protein coding potential, which have been already demonstrated to play pivotal roles within cells, being involved in different processes, such as proliferation, cell cycle regulation, apoptosis, migration, and diseases, including cancer. Accordingly, they could be used as targets for future TNBC personalized therapy. Moreover, the peculiar characteristics of non-coding RNAs make them reliable biomarkers to monitor cancer treatment, thus, to monitor recurrence or chemoresistance, which are the most challenging aspects in TNBC. In the present review, we focused on the oncogenic or oncosuppressor role of long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) mostly involved in TNBC, highlighting their mode of action and depicting their potential role as a biomarker and/or as targets of new non-coding RNA-based therapeutics. [ABSTRACT FROM AUTHOR]

Researchers studying Amyotrophic Lateral Sclerosis (ALS) have made significant efforts to find a unique mechanism to explain the etiopathology of the different forms of the disease. However, despite several mutations associated with ALS having been discovered in recent years, the link between the mutated genes and its onset has not yet been fully elucidated. Among the genes associated with ALS, superoxide dismutase 1 (SOD1) was the first to be identified, but its role in the etiopathogenesis of the disease is still unclear. In recent years, research has been focused on the non-coding part of the genome to fully understand the mechanisms underlying gene regulation. Non-coding RNAs are conserved molecules and are not usually translated in protein. A total of 98% of the human genome is composed of non-protein coding sequences with roles in the transcriptional and post-transcriptional regulation of gene expression. In this study, we characterized a divergent nuclear lncRNA (SOD1-DT) transcribed in the antisense direction from the 5′ region of the SOD1 coding gene in both the SH-SY5Y cell line and fibroblasts derived from ALS patients. Interestingly, this lncRNA seems to regulate gene expression, since its inhibition leads to the upregulation of surrounding genes including SOD1. SOD1-DT represents a very complex molecule, displaying allelic and transcriptional variability concerning transposable elements (TEs) included in its sequence, widening the scenario of gene expression regulation in ALS disease. [ABSTRACT FROM AUTHOR]

Purpose: Renal cell carcinoma belongs among the deadliest malignancies despite great progress in therapy and accessibility of primary care. One of the main unmet medical needs remains the possibility of early diagnosis before the tumor dissemination and prediction of early relapse and disease progression after a successful nephrectomy. In our study, we aimed to identify novel diagnostic and prognostic biomarkers using next-generation sequencing on a novel cohort of RCC patients. Methods: Global expression profiles have been obtained using next-generation sequencing of paired tumor and non-tumor tissue of 48 RCC patients. Twenty candidate lncRNA have been selected for further validation on an independent cohort of paired tumor and non-tumor tissue of 198 RCC patients. Results: Sequencing data analysis showed significant dysregulation of more than 2800 lncRNAs. Out of 20 candidate lncRNAs selected for validation, we confirmed that 14 of them are statistically significantly dysregulated. In order to yield better discriminatory results, we combined several best performing lncRNAs into diagnostic and prognostic models. A diagnostic model consisting of AZGP1P1, CDKN2B-AS1, COL18A1, and RMST achieved AUC 0.9808, sensitivity 95.96%, and specificity 90.4%. The model for prediction of early relapse after nephrectomy consists of COLCA1, RMST, SNHG3, and ZNF667-AS1 and achieved AUC 0.9241 with sensitivity 93.75% and specificity 71.07%. Notably, no combination has outperformed COLCA1 alone. Lastly, a model for stage consists of ZNF667-AS1, PVT1, RMST, LINC00955, and TCL6 and achieves AUC 0.812, sensitivity 85.71%, and specificity 69.41%. Conclusion: In our work, we identified several lncRNAs as potential biomarkers and developed models for diagnosis and prognostication in relation to stage and early relapse after nephrectomy. [ABSTRACT FROM AUTHOR]

Background: Dysregulation of Long Non-coding RNAs (lncRNAs) emerges to be a hallmark of cancers. Metastatic prostate cancer and localized disease that recurs after treatment are clinical challenges, it remains unclear how lncRNA plays a role in those processes. Methods: From previous RNA-Seq data on 65 prostate cancer and adjacent normal tissues. We identified a novel lncRNA ENST00000503625 down-regulated in prostate cancer and correlated with tumor progression characteristics. Public datasets were examined for associations between ENST00000503625 expression and clinical parameters and prognoses. Subsequently, we constructed and externally validated a nomogram for predicting biochemical recurrence (BCR). Finally, in vitro experiments were carried out to determine how ENST00000503625 functions biologically in prostate cancer. Results: Low ENST00000503625 in tumor was associated with poor clinical features and prognoses. TCGA pan-cancer analysis found that ENST00000503625 was deregulated in a variety of tumors and correlated with overall survival, disease-specific survival, and progression-free survival. The nomogram for predicting BCR was constructed using TCGA data, which exhibited excellent accuracy in external validation with Chinese Prostate Cancer Genome and Epigenome Atlas data. Gene Ontology and KEGG pathway analysis found that genes related to ENST00000503625 were enriched in multiple tumor progression related pathways. When ENST00000503625 was knocked down in vitro, the epithelial-mesenchymal transition was induced, by which cancer cells migrated and invaded more readily. Conclusion: Our data suggested that ENST00000503625 may serve as a potential prognostic marker or a therapeutic target for prostate cancer metastases. [ABSTRACT FROM AUTHOR]

Background: An increasing amount of research has speculated that necroptosis could be a therapeutic strategy for treating cancer. However, understanding the prognostic value of the necroptosis-related long non-coding RNAs (NRLs) in skin cutaneous melanoma (SKCM, hereafter referred to as melanoma) remains poor and needs to be developed. Our research aims to construct a model based on NRLs for the prognosis of patients with melanoma. Methods: We obtained the RNA-seq and clinical data from The Cancer Genome Atlas (TCGA) database and retrieved 86 necroptosis-related genes from the GeneCards database. The lncRNAs associated with necroptosis were identified via the Pearson correlation coefficient, and the prognostic model of melanoma was constructed using LASSO regression. Next, we employed multiple approaches to verify the accuracy of the model. Melanoma patients were categorized into two groups (high-risk and low-risk) according to the results of LASSO regression. The relationships between the risk score and survival status, clinicopathological correlation, functional enrichment, immune infiltration, somatic mutation, and drug sensitivity were further investigated. Finally, the functions of AL162457.2 on melanoma proliferation, invasion, and migration were validated by in vitro experiments. Results: The prognostic model consists of seven NRLs (EBLN3P, AC093010.2, LINC01871, IRF2-DT, AL162457.2, AC242842.1, HLA-DQB1-AS1) and shows high diagnostic efficiency. Overall survival in the high-risk group was significantly lower than in the low-risk group, and risk scores could be used to predict melanoma survival outcomes independently. Significant differences were evident between risk groups regarding the expression of immune checkpoint genes, immune infiltration, immunotherapeutic response and drug sensitivity analysis. A series of functional cell assays indicated that silencing AL162457.2 significantly inhibited cell proliferation, invasion, and migration in A375 cells. Conclusion: Our prognostic model can independently predict the survival of melanoma patients while providing a basis for the subsequent investigation of necroptosis in melanoma and a new perspective on the clinical diagnosis and treatment of melanoma. [ABSTRACT FROM AUTHOR]

Background: Long non-coding RNAs (lncRNAs) are defined as transcribed molecules longer than 200 nucleotides with little to no protein-coding potential. LncRNAs can regulate gene expression of nearby genes (cis-acting) or genes located on other chromosomes (trans-acting). Several methodologies have been developed to capture lncRNAs associated with chromatin at a genome-wide level. Analysis of RNA-DNA contacts can be combined with epigenetic and RNA-seq data to define potential lncRNAs involved in the regulation of gene expression. Results: We performed Chromatin Associated RNA sequencing (ChAR-seq) in Anolis carolinensis to obtain the genome-wide map of the associations that RNA molecules have with chromatin. We analyzed the frequency of DNA contacts for different classes of RNAs and were able to define cis- and trans-acting lncRNAs. We integrated the ChAR-seq map of RNA-DNA contacts with epigenetic data for the acetylation of lysine 16 on histone H4 (H4K16ac), a mark connected to actively transcribed chromatin in lizards. We successfully identified three trans-acting lncRNAs significantly associated with the H4K16ac signal, which are likely involved in the regulation of gene expression in A. carolinensis. Conclusions: We show that the ChAR-seq method is a powerful tool to explore the RNA-DNA map of interactions. Moreover, in combination with epigenetic data, ChAR-seq can be applied in non-model species to establish potential roles for predicted lncRNAs that lack functional annotations. [ABSTRACT FROM AUTHOR]

Tens of thousands of long non-coding RNAs have been uncovered in plants, but few of them have been comprehensively studied for their biological function and molecular mechanism of their mode of action. Here, we show that the Arabidopsis long non-coding RNA DANA2 interacts with an AP2/ERF transcription factor ERF84 in the cell nucleus and then affects the transcription of JMJ29 that encodes a Jumonji C domain-containing histone H3K9 demethylase. Both RNA sequencing (RNA-seq) and genetic analyses demonstrate that DANA2 positively regulates drought stress responses through JMJ29. JMJ29 positively regulates the expression of ERF15 and GOLS2 by modulation of H3K9me2 demethylation. Accordingly, mutation of JMJ29 causes decreased ERF15 and GOLS2 expression, resulting in impaired drought tolerance, in agreement with drought-sensitive phenotypes of dana2 and erf84 mutants. Taken together, these results demonstrate that DANA2 is a positive regulator of drought response and works jointly with the transcriptional activator ERF84 to modulate JMJ29 expression in plant response to drought. This study identifies a long non-coding RNA, DANA2 , that positively regulates drought tolerance in Arabidopsis. DANA2 works jointly with the transcriptional activator ERF84 to regulate JMJ29 expression, thereby modulating JMJ29 chromatin enrichment at the ERF15 and GOLS2 loci and altering their expression during drought response. [ABSTRACT FROM AUTHOR]

Background: Breast cancer (BRCA) has become the most diagnosed cancer worldwide for female and seriously endanger female health. The epithelialmesenchymal transition (EMT) process is associated with metastasis and drug resistance in BRCA patients. However, the prognostic value of EMT-related lncRNA in BRCA still needs to be revealed. The aim of this study is to construct an EMT-related lncRNA (ERL) signature with accuracy predictive ability for the prognosis of BRCA patients. Methods: RNA-seq expression data and Clinical characteristics obtained from the TCGA (The Cancer Genome Atlas) were used in the study. First, we identified the EMT-related lncRNA by the Pearson correlation analysis. An EMT-related lncRNAs prognostic risk signature was constructed using univariate Cox regression and Lasso-penalized Cox regression analyses. The model’s performance was validated using Kaplan-Meier (KM) survival analysis, ROC curve and C-index. Finally, a nomogram was constructed for clinical practice in evaluating the patients with BRCA and validated by calibration curve and decision curve analysis (DCA). We also evaluated the drug sensitivity of signature lncRNA and the tumor immune cell infiltration in breast cancer. Results: We constructed a 10-lncRNA risk score signature based on the lncRNAs associated with the EMT process. We could assign BRCA patients to the highand low-risk group according to the median risk score. The prognostic risk signature showed excellent accuracy and demonstrated sufficient independence from other clinical characteristics. The immune cell infiltration analysis showed that the prognostic risk signature was related to the infiltration of the immune cell subtype. Drug sensitivity analysis proved ERLs signature could effectively predict the sensitivity of patients to common chemotherapy drugs in BRCA and provide guidance for chemotherapy drugs for high-risk and low-risk patients. Conclusion: Our ERL signature and nomogram have excellent prognostic value and could become reliable tools for clinical guidance. [ABSTRACT FROM AUTHOR]

Introduction: Immune thrombocytopenia (ITP) is a common acquired hemorrhagic disease without "gold standard" for the diagnosis, long non‐coding RNA (lncRNAs) can participate in regulating gene expression through various mechanisms and may play a role in immune intolerance in ITP. Several previous studies have confirmed that lncRNA lncDC and THRIL are involved in the development of autoimmune diseases. This study investigates the relationship between expression levels of two plasma lncRNAs (lncDC and THRIL) and clinical characteristics of adult primary ITP patients, ascertain their potential applications as diagnostic markers of ITP. Methods: We recruited 102 subjects, including 41 ITP patients, 41 healthy controls (HCs) and 20 patients under myelosuppression phase after chemotherapy (MS). qRT‐PCR was used to detect the expression of two lncRNAs in the peripheral blood plasma of the three groups. Receiver operating characteristic (ROC) curves were used to test the diagnostic efficacy of lncDC and THRIL in ITP. Results: The expression level of lncDC was downregulated in ITP patients compared with HCs (p =. 012) and MS (p =.035), whereas THRIL was significantly upregulated (p =.0005, p <. 0001). We further revealed that lncDC has a high sensitivity (78. 05%), while THRIL has a high specificity (97. 56%). The area under the curve (AUC) (0.869, 95% CI: 0.795–0.943, p <.0001) of the ROC curve for this combination increased significantly. Conclusions: THRIL and lncDC expression levels were changed in adult ITP patients. The lncRNAs lncDC and THRIL can serve as potential diagnostic markers for adult primary ITP. [ABSTRACT FROM AUTHOR]

Tuberculosis (TB), one of the top ten causes of death globally induced by the infection of Mycobacterium tuberculosis (Mtb), remains a grave public health issue worldwide. With almost one-third of the world's population getting infected by Mtb, between 5% and 10% of these infected individuals are predicted to develop active TB disease, which would not only result in severe tissue damage and necrosis, but also pose serious threats to human life. However, the exact molecular mechanisms underlying the pathogenesis and immunology of TB remain unclear, which significantly restricts the effective control of TB epidemics. Despite significant advances in current detection technologies and treatments for TB, there are still no appropriate solutions that are suitable for simultaneous, early, rapid, and accurate screening of TB. Various cellular events can perturb the development and progression of TB, which are always associated with several specific molecular signaling events controlled by dysregulated gene expression patterns. Long non-coding RNAs (lncRNAs), a kind of non-coding RNA (ncRNA) with a transcript of more than 200 nucleotides in length in eukaryotic cells, have been found to regulate the expression of protein-coding genes that are involved in some critical signaling events, such as inflammatory, pathological, and immunological responses. Increasing evidence has claimed that lncRNAs might directly influence the susceptibility to TB, as well as the development and progression of TB. Therefore, lncRNAs have been widely expected to serve as promising molecular biomarkers and therapeutic targets for TB. In this review, we summarized the functions of lncRNAs and their regulatory roles in the development and progression of TB. More importantly, we widely discussed the potential of lncRNAs to act as TB biomarkers, which would offer new possibilities in novel diagnostic strategy exploration and benefit the control of the TB epidemic. [ABSTRACT FROM AUTHOR]

Recent studies demonstrated that short open reading frames (sORFs, <100 codons) can encode the peptides or microproteins that perform important functions in prokaryotic and eukaryotic cells. It was established that the products of sORF translation are involved in the regulation of many processes; for example, they modulate the activity of the mitochondrial respiratory chain or the activity of muscle cells in mammals. However, the identification and subsequent functional analysis of the peptides or microproteins encoded by sORF is a nontrivial task that requires the use of special approaches. The discovery of partner proteins for the studied peptide is one of the critical stages in functional analysis. This review considers the peculiarities of the analysis of the interactome of sORF-encoded microproteins and describes the approaches currently used for such studies. [ABSTRACT FROM AUTHOR]

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]

Recent advances in RNA sequencing technologies helped uncover what was once uncharted territory in the human genome—the complex and versatile world of long noncoding RNAs (lncRNAs). Previously thought of as merely transcriptional "noise", lncRNAs have now emerged as essential regulators of gene expression networks controlling development, homeostasis and disease progression. The regulatory functions of lncRNAs are broad and diverse, and the underlying molecular mechanisms are highly variable, acting at the transcriptional, post-transcriptional, translational, and post-translational levels. In recent years, evidence has accumulated to support the important role of lncRNAs in the development and functioning of the lymphatic vasculature and associated pathological processes such as tumor-induced lymphangiogenesis and cancer metastasis. In this review, we summarize the current knowledge on the role of lncRNAs in regulating the key genes and pathways involved in lymphatic vascular development and disease. Furthermore, we discuss the potential of lncRNAs as novel therapeutic targets and outline possible strategies for the development of lncRNA-based therapeutics to treat diseases of the lymphatic system. [ABSTRACT FROM AUTHOR]

Coronary artery disease (CAD) is a leading cause of mortality worldwide. In this study, we aimed to assess the potential of plasma long non-coding RNAs (lncRNAs) LIPCAR and MALAT1 and microRNAs (miRNAs) miR-142-3p and miR-155-5p to discriminate unstable CAD patients from stable ones. 23 stable angina (SA), 21 unstable angina (UA), and 50 ST-segment elevation myocardial infarction (STEMI) patients were enrolled; their plasma was collected. ncRNA plasma levels were evaluated using RT-qPCR. All measured ncRNA levels were significantly increased in UA patients' plasma compared to SA patients' plasma and in STEMI-with major adverse cardiovascular event (MACE) patients' plasma vs. STEMI-without MACE patients' plasma. ROC analysis showed that increased levels of LIPCAR and MALAT1 were associated with UA, and the prognostic model improved with the addition of miR-155-5p levels. The assessed lncRNAs discriminated between hyperglycemic (HG) and normoglycemic (NG) UA patients, and they were associated with MACE incidence in STEMI patients; this prediction was improved by the addition of miR-142-3p levels to the ROC multivariate model. We propose LIPCAR and MALAT1 as effective diagnostic markers for vulnerable CAD, their association with HG in UA patients, and as robust predictors for unfavorable evolution of STEMI patients. [ABSTRACT FROM AUTHOR]

Skin cutaneous melanoma (SKCM) is the most malignant skin tumor for it is enormously easy to develop invasion and metastasis. Autophagy is a process by which cellular material is degraded by lysosomes or vacuoles and recycled. Autophagy-related long non-coding RNAs (lncRNAs) have been thought to correlate with SKCM. This study aims to explore the prognostic significance of autophagy-related lncRNAs and establish a prognostic model of autophagy-related lncRNA pairs in SKCM. Firstly, the RNA-seq data and related clinical information were downloaded from the TCGA database. 446 qualified samples were enrolled. 222 autophagy-related genes were obtained from the HADb database. Pearson correlation analysis was conducted to identify autophagy-related lncRNAs (ARLs). After that, we obtained prognosis-related ARLs and autophagy-related lncRNA pairs (ARLPs). Using Lasso-Cox regression analysis, an autophagy-related lncRNA-pair prognostic signature was established. The accuracy of the signature were confirmed through a series of validations in terms of mutation profiles, immunity infiltration, and cellular pathways. And we used the random forest method to find USP30-AS1 as a key mediating factor in SKCM. [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]

COVID-19, an acute respiratory syndrome caused by the SARS-CoV-2 virus, was first reported in late 2019 in Wuhan, China, and rapidly escalated into a global pandemic. The condition can lead to organ dysfunction and, ultimately, death through acute respiratory distress syndrome (ARDS). Disease severity has been linked to proinflammatory cytokines, which activate the NF-κB and STAT transcription factors in infected cells. It has been proven that lncRNAs play an essential role in reducing or increasing inflammatory factors. This makes them potentially valuable in recognizing pathogenesis pathways and therapeutic targets in COVID-19. Nanocurcumin is known as an antioxidant, tumor suppressor, and anti-inflammatory substance, and it can be effective in reducing inflammation caused by the disease of COVID-19. This study analyzed Sequence Read Archive data from COVID-19 patients with acute versus milder symptoms, identifying dysregulated genes and noncoding RNAs. To verify this correlation, the expression of the candidate gene was evaluated with quantitative polymerase chain reaction (qPCR) in mouse models, while immunoglobulin (Ig) G titer was measured using enzyme-linked immunosorbent assay (ELISA) in mouse serum samples. Here, we introduced a novel lncRNA called HSD17B3-AS1, suggested as a therapeutic target in COVID-19 patients with acute symptoms. Furthermore, we revealed that nanocurcumin reduces the expression of HSD17B3-AS1, which leads to reduced inflammation in mice. These results suggest that HSD17B3-AS1 plays a significant regulatory role in managing COVID-19, and the downregulation of HSD17B3-AS1 by Nanocurcumin presents a promising treatment option for minimizing complications in COVID-19 patients. [ABSTRACT FROM AUTHOR]

Non-coding RNAs (ncRNAs) are important regulators of gene expression. They are expressed not only in cells, but also in cell-derived extracellular vesicles (EVs). The mechanisms controlling their loading and sorting remain poorly understood. Here, we investigated the impact of TP53 mutations on the non-coding RNA content of small melanoma EVs. After purification of small EVs from six different patientderived melanoma cell lines, we characterized them by small RNA sequencing and lncRNA microarray analysis. We found that TP53 mutations are associated with a specific micro and long non-coding RNA content in small EVs. Then, we showed that long and small non-coding RNAs enriched in TP53 mutant small EVs share a common sequence motif, highly similar to the RNA-binding motif of Sam68, a protein interactingwith hnRNP proteins. This protein thus may be an interesting partner of p53, involved in the expression and loading of the ncRNAs. To conclude, our data support the existence of cellular mechanisms associate with TP53 mutations which control the ncRNA content of small EVs in melanoma. [ABSTRACT FROM AUTHOR]

Introduction: This prospective observational study with a control group aimed to compare the plasma levels of long non-coding RNA (lncRNA) LIPCAR between patients with acute cerebral infarction (ACI) and healthy controls, and to assess the prognostic abilities of LIPCAR for adverse outcomes of patients with ACI at 1-year follow-up. Methods: Eighty patients with ACI, of whom 40 had large artery atherosclerosis (LAA) and 40 had cardioembolism (CE) and who were hospitalized at Xi'an No. 1 Hospital from July 2019 to June 2020, were selected as the case group. Age- and sex-matched non-stroke patients from the same hospital throughout the same time period were chosen as the control group. Real-time quantitative reverse transcription polymerase chain reaction was used to measure the levels of plasma lncRNA LIPCAR. The correlations of LIPCAR expression among the LAA, CE, and control groups were assessed using Spearman's correlation analysis. Curve fitting and multivariate logistic regression were used to analyze the LIPCAR levels and 1-year adverse outcomes of patients with ACI and its subtypes. Results: The expression of plasma LIPCAR in the case group was noticeably higher than that of the control group (2.42 ± 1.49 vs. 1.00 ± 0.47, p < 0.001). Patients with CE had considerably higher levels of LIPCAR expression than those with LAA. The National Institute of Health Stroke Scale score and modified Rankin scale score on admission were significantly positively correlated with LIPCAR expression in patients with CE and LAA. Furthermore, the correlation was stronger in patients with CE than in those with LAA, with correlation coefficients of 0.69 and 0.64, respectively. Curve fitting revealed a non-linear correlation between LIPCAR expression levels, 1-year recurrent stroke, all-cause mortalities, and poor prognoses, with a cut-off value of 2.2. Conclusion: The expression level of lncRNA LIPCAR may play a potential role in the identification of neurological impairment and CE subtype in patients with ACI. Increased 1-year risk of adverse outcomes may be associated with high levels of LIPCAR expression. Plain Language Summary: Acute cerebral infarction is the second-leading cause of death worldwide. Therefore, available diagnostic and prognostic tools are of the utmost importance. It is easy to acquire hematologic biomarkers and to provide direct information related to the severity of brain injury and the risk of stroke. However, it has been shown that the study of hematologic markers in aspects of both identifying stroke subtypes and predicting neurological impairment are still few and imperfect in clinical application of stroke prognosis. The long non-coding RNA LIPCAR plays an important role in the pathophysiology of cardiovascular disease. Nonetheless, to date, no exploration has been carried out on the correlation between lncRNA LIPCAR, severity on admission, and prognosis of stroke subtypes. Thus, this study aimed to investigate the plasma levels of lncRNA LIPCAR expression and their correlations in patients with acute cerebral infarction and its subtypes. Our results show that the plasma levels of LIPCAR expression of the patients with acute cerebral infarction were noticeably higher than those of the non-stroke control patients. Patients with cardioembolism subtype had considerably higher levels of LIPCAR expression than those with large artery atherosclerosis. The National Institute of Health Stroke Scale score and modified Rankin scale score on admission were significantly correlated with LIPCAR expression in patients with cardioembolism and large artery atherosclerosis; the correlation was stronger in patients with cardioembolism than in patients with large artery atherosclerosis, with correlation coefficients of 0.69 and 0.64, respectively. Furthermore, curve fitting revealed a non-linear correlation between LIPCAR expression levels and 1-year outcome events. The expression level of lncRNA LIPCAR may play a potential role in the identification of neurological impairment and cardioembolism subtype in patients with acute cerebral infarction. [ABSTRACT FROM AUTHOR]