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Eph receptors tyrosine kinase (RTK) were identified in 1987 from hepatocellular carcinoma cell lines and were the largest known subfamily of RTK. Eph receptors can be divided into two categories, EphA and EphB, based on their structure and receptor-ligand specificity. EphA can be divided into 10 species (EphA 1-10), and EphB into 6 species (EphB1-6). Similarly, the ligands of Eph receptors are Ephrins. Ephrins also can be divided into Ephrin A and Ephrin B, of which there are five species(Ephrin-A1-5) and three species(Ephrin-B1-3). Among the Eph receptors, EphA1 has been the least studied so far. As far as we know, Eph receptors are involved with multiple pathologies, including cancer progression, tumor angiogenesis, intestinal environmental stability, the lymph node system, neurological disease, and inhibition of nerve regeneration after injury. There is a link between EphA1, integrin and ECM- related signal pathways. Ephrin-A1 is a ligand of the EphA1 receptor. EphA1 and ephrin-A1 functions are related to tumor angiogenesis. EphA1 and ephrin-A1 also play roles in gynecological diseases. Ephrin-A1 and EphA1 receptor regulate follicular formation, ovulation, embryo transport, implantation and placental formation, which are of great significance for the occurrence of gynecological tumor diseases. EphA1 has been identified as an oncoprotein in various tumors, and is associated with the prognosis of a variety of tumors in recent years. EphA1 is considered a driver gene in tumor genomics. There are significant differences in EphA1 expression levels in different types of normal tissues and tumors, and even in different stages of tumor development, suggesting its functional diversity. Changes at the gene level in cell biology are often used as biological indicators of cancer, known as biomarkers, which can be used to provide diagnostic or prognostic information and are valuable for improving the detection, monitoring and treatment of tumors. However, few prognostic markers can selectively predict clinically significant tumors with poor prognosis. These malignancies are more likely to progress and lead to death, requiring more aggressive treatment. Currently available treatments for advanced cancer are often ineffective, and treatment options are mainly palliative. Therefore, early identification and treatment of those at risk of developing malignant tumors are crucial. Although pieces of evidence have shown the role of EphA1 in tumorigenesis and development, its specific mechanism is still unknown to a great extent.This review reveals the changes and roles of EphA1 in many tumors and cancers. The change of EphA1 expression can be used as a biological marker of cancer, which is valuable for improving tumor detection, monitoring and treatment, and can be applied to imaging. Studies have shown that structural modification of EphA1 could make it an effective new drug. EphA1 is unique in that it can be considered a prognostic marker in many tumors and is of important meaning for clinical diagnosis and operative treatment. At the same time, the study of the specific mechanism of EphA1 in tumors can provide a new way for targeted therapy.Relevant studies were retrieved and collected through the PubMed system. After determining EphA1 as the research object, by analyzing research articles on EphA1 in the PubMed system in recent 10 years, we found that EphA1 was closely connected with the occurrence and development of tumors, and further determined the references according to the influencing factors for review and analysis.EphA1 has been identified as a cancer protein in various tumors, such as hepatocellular carcinoma, nasopharyngeal carcinoma, ovarian cancer, gastric cancer, colorectal cancer, clear cell renal cell carcinoma, esophageal squamous cell carcinoma, breast cancer, prostate cancer and uveal melanoma. EphA1 is abnormally expressed in these tumor cells, which mainly plays a role in cancer progression, tumor angiogenesis, intestinal environmental stability, the lymph node system, nervous system diseases and gynecological diseases. In a narrow sense, EphA1 is especially effective in breast cancer in terms of gynecological diseases. However, the specific mechanism of EphA1 leading to the change of cancer cells in some tumors is not clear, which needs further research and exploration.RTK EphA1 can be used as a biomarker for tumor diagnosis (especially a prognostic marker), an indispensable therapeutic target for new anti-tumor therapies, and a novel anti-tumor drug.

Abstract: Nonalcoholic fatty liver disease (NAFLD) has received worldwide scientific attention because of its rapidly increasing prevalence, and it has emerged as a serious public health problem in end-stage liver disease. Many factors are involved in the multifactorial development and progression of liver disease by influencing multiple signaling and metabolic pathways. Currently, many studies have demonstrated the critical role of microRNA- 21 (miR-21) in NAFLD pathogenesis. In addition, many studies have found that miR-21 is highly expressed in inflammatory bowel disease, which is associated with intestinal barrier dysfunction and altered gut microbiota. In this paper, we focus on the regulatory role of miR-21 in the progression of NAFLD and its effect on the gut microbiota, summarize the involvement of miR-21 through a variety of signaling pathways and metabolic pathways, as well as discuss some predicted miR-21 target genes and miR-21 pathways for future experimental identification.

Abstract: Long non-coding RNA has attracted the interest of researchers as a relevant factor that can influence human cancers. As an oncogene and suppressor gene, it has numerous pathways and is closely related to the pathophysiology of human diseases. Meanwhile, it may become a novel treatment option and target for tumor treatment. CRNDE is the gene symbol for Colorectal Neoplasia Differentially Expressed (non-protein-coding) since it was found to be considerably higher in colorectal cancer when it was first discovered. It's transcribed from human chromosome 16. Many studies have shown that it is intimately linked to the etiology of many tumors and malignancies. According to the paper, the biological function and pathophysiological mechanism of CRNDE in tumors have been studied extensively in recent years. PubMed served as an essential platform for conducting literature searches and related analyses. CRNDE, a long non-coding RNA closely related to tumors, was highly expressed in many tumor cells. There were various underlying mechanisms affecting the progression of CRNDE-regulated tumorigenesis, including hepatocellular carcinoma, gastric cancer, prostate carcinoma, oral squamous cell carcinoma, breast cancer, thyroid cancer, myeloma, leukemia, melanoma, colorectal cancer, glioblastoma, osteosarcoma, cervical cancer, intrahepatic cholangiocarcinoma, nonsmall cell lung cancer, hepatoblastoma cell tumor, abdominal aortic aneurysm, nasopharyngeal carcinoma, bladder cancer, Wilms tumor, medulloblastoma, pancreatic cancer, gallbladder cancer, ovarian cancer, and renal cell carcinoma. CRNDE is involved in the processes of proliferation, migration, invasion, and inhibition of apoptosis of various cancer cells.

Background: It is well known that the changes in the expression level of LncRNA can affect the progression of tumors, which has caused a great upsurge of research in recent years. Several LncRNAs have been identified to affect a series of cancers and can promote tumor growth, migration, and invasion. In this review, we aim to clarify the pathophysiological functions of LncRNA MIR4435-2 HG in multiple tumors. Methods: By searching the literature through PubMed, this paper summarizes the relationship between MIR4435-2HG and tumor and its role in the occurrence and development of cancer and also explains the specific molecular mechanism of the effect of MIR4435-2HG on cancer. Results: MIR4435-2HG can function as an oncogene in a variety of cancers. The expression level was reported to be abnormally elevated in a series of cancers, consisting of melanoma, gastric cancer, head and neck squamous cell carcinoma, oral squamous cell carcinoma, lung cancer, cervical cancer, prostate carcinoma, ovarian cancer, breast cancer, hepatocellular carcinoma, clear cell renal cell carcinoma malignant, glioma, and colorectal cancer. Moreover, MIR4435-2HG is related to the poor prognosis of a variety of cancers. MIR4435-2HG can also affect tumor proliferation, invasion, and apoptosis. In addition, MIR4435-2HG can also enhance the metabolic function of myeloid dendritic cells of elite HIV-1 controllers. Conclusion: MIR4435-2HG affects the development of a variety of cancers. It can act as a clinical marker for early tumor diagnosis and affects tumor-targeted therapy.

Abstract: Long non-coding RNA (lncRNA) is a new kind of RNA with a length of over 200 nucleotides. Current frontiers revealed that lncRNAs implicate in various tumor progression, including tumorigenesis, proliferation, migration, invasion, metastasis, and angiogenesis. Recently discovered long non-coding RNA SETbinding factor 2 antisense RNA 1 (lncRNA SBF2-AS1), an oncogenic antisense RNA to SBF2, locates at 11p15.1 locus and is 2708 nt long. Accumulating evidence has demonstrated that lncRNA SBF2-AS1 participates in the progression of the various tumor, including pathogenesis, diagnosis, treatment, and prognosis of acute myeloid leukemia (AML), breast cancer (BC), cervical cancer (CC), clear cell renal cell carcinoma (ccRCC), colorectal cancer (CRC), diffuse large B-cell lymphoma (DLBCL), esophageal squamous cell carcinoma (ESCC), gastric cancer (GC), glioma, glioblastoma (GBM), hepatocellular carcinoma (HCC), lung cancer (LC), lung adenocarcinoma (LUAD), non-small cell lung cancer (NSCLC), osteosarcoma (OS), pancreatic cancer (PC), papillary thyroid cancer (PTC), small cell lung cancer (SCLC). Therefore, we summarized the underlying mechanisms of lncRNA SBF2-AS1 in various cancers to utilize its therapeutic function in target-selective treatment modalities.

Background: FER-1 family member 4 (FER1L4), a 6.7 kb lncRNA located at 20q11.22, plays an important biological function in a variety of tumor diseases. The purpose of this review is to clarify the pathophysiological mechanism and potential biological function of FER1L4 in different tumors. Methods: By searching the relevant literature in PubMed, the specific pathophysiological mechanism of FER1L4 in different tumors was summarized. Results: LncRNA FER1L4 is one of the key factors in tumorigenesis and is abnormally down-regulated in many tumors, including osteosarcoma, lung cancer, laryngeal squamous cell carcinoma, laryngeal cancer, colorectal cancer, ovarian cancer, prostate cancer, esophageal cancer, gastric cancer, endometrial cancer, osteoarthritis, rheumatoid arthritis, and so on. However, FER1L4 is downregulated in breast cancer, glioma, oral squamous cell carcinoma, renal clear cell carcinoma, and periodontitis, and plays a protective role in orthodontic teeth. In addition, as a tumor suppressor gene or oncogene, FER1L4 affects tumor proliferation, invasion, migration, and apoptosis. Conclusion: LncRNA FER1L4 has a good application prospect in the treatment and diagnosis of various tumors.

Abstract: Aging refers to a natural process and a universal phenomenon in all cells, tissues, organs, and the whole organism. Long non-coding RNAs (lncRNAs) are non-coding RNAs with a length of 200 nucleotides. LncRNA growth arrest-specific 5 (lncRNA GAS5) is often down-regulated in cancer. The accumulation of lncRNA GAS5 has been found to be able to inhibit cancer growth, invasion, and metastasis while enhancing the sensitivity of cells to chemotherapy drugs. LncRNA GAS5 can be a signaling protein, which is specifically transcribed under different triggering conditions. Subsequently, it is involved in signal transmission in numerous pathways as a signal node. LncRNA GAS5, with a close relationship to multiple miRNAs, was suggested to be involved in the signaling pathway under three action modes (i.e., signal, bait, and guidance). LncRNA GAS5 was found to be involved in different age-related diseases (e.g., rheumatoid arthritis, type 2 diabetes, atherosclerosis, osteoarthritis, osteoporosis, multiple sclerosis, cancer, etc.). This study mainly summarized the regulatory effect exerted by lncRNA GAS5 on age-related diseases.

Abstract: LncRNA MIR17HG, located at chromosome 13q31, plays an inevitable role in promoting tumor progressions, such as tumorigenesis, proliferation, and metastasis. Besides, lncRNA MIR17HG is rare due to its open reading frame (ORF), which can be translated to produce protein. By systematically retrieval, we summarized that MIR17HG is an emerging lncRNA that exhibits carcinogenically in osteosarcoma (OS), glioma, cervical squamous cell carcinoma (CSCC), colorectal cancer (CRC), gastric cancer (GC), atypical teratoid rhabdoid tumors (ATRT). Furthermore, a high expression level of MIR17HG protein is also linked with meningioma. Additionally, MIR17HG polymorphisms in glioma, CRC, liver cancer (LC), breast cancer (BC), head and neck squamous cell carcinoma (HNSCC), and multiple myeloma (MM) also have a large influence on cancer susceptibility, prognosis, and so on. Collectively, long non-coding RNA MIR17HG’s tumor-stimulative role could be a promising therapeutic target. Besides, by investigating patients’ MIR17HG single-nucleotide polymorphisms (SNPs), clinicians could also personalize the productive interventions in gene therapy or predict the diagnosis/prognosis precisely.

Background: Nuclear‐enriched abundant transcript 1 (abbreviated as NEAT1) is a long-chain noncoding RNA involved in various physiological and pathological processes. This study aimed to clarify the effect and molecule system of NEAT1 within non-alcoholic fatty liver disease (NAFLD) as well as type 2 diabetes (T2DM). Method: In this review, current studies concerning mechanisms of NEAT1l, in the development of type 2 diabetes and its complications have been summarized and analyzed. Also, we searched the papers based on NEAT1 related to NAFLD. The related studies were obtained through a systematic search of Pubmed. Results: NEAT1 displays a close correlation with how T2DM occurs and develops, and it was confirmed to be significantly up-regulated in T2DM and its various complications (e.g., diabetics nephropathy, diabetics cardiomyopathy, diabetics retinopathy as well as diabetic neuropathy). Besides, NEAT1 is capable of impacting the occurrence, development and prognosis of NAFLD and T2DM. Conclusion: LncRNA NEAT1 is likely to act as a novel therapeutic target for T2DM and its complications. Moreover, non-alcoholic fatty liver disease is also correlated with NEAT1.

Background Diabetes is now afflicting an expanding population, and it has become a major source of concern for human health. Diabetes affects several organs and causes chronic damage and dysfunction. It is one of the three major diseases that are harmful to human health. Plasmacytoma variant translocation 1 is a member of long non-coding RNA. PVT1 expression profile abnormalities have been reported in diabetes mellitus and its consequences in recent years, suggesting that it may contribute to the disease's progression. Methods Relevant literature from the authoritative database “PubMed” are retrieved and summarized in detail. Results Mounting evidence reveals that PVT1 has multiple functions. Through sponge miRNA, it can participate in a wide variety of signal pathways and regulate the expression of a target gene. More importantly, PVT1 is crucially implicated in the regulation of apoptosis, inflammation, and so on in different types of diabetes-related complications. Conclusion PVT1 regulates the occurrence and progression of diabetes-related diseases. Collectively, PVT1 has the potential to be a useful diagnostic and therapeutic target for diabetes and its consequences.

Background: Increasing academic efforts have been made to explore the correlation of long noncoding RNAs (lncRNAs) with human diseases, particularly metabolic diseases like diabetes mellitus. Taking lncRNA H19 as an example, this review intends to reveal the functions and mechanism of lncRNA H19 in diabetes mellitus and diabetic complications. Methods: The research results associated with lncRNA H19 and diabetes mellitus are collected and summarized on PubMed. Conclusion: LncRNA H19 is a potential instructive marker for the treatment of diabetes mellitus and diabetic complications.

Background: NR2F1-AS1 is a long non-coding RNA (lnc RNA) that is involved in different biological processes. It plays an integral role in the pathophysiology of human diseases, especially tumorigenesis and progression. Therefore, it may be a promising target for numerous tumor biotherapeutics. The current review study aimed to show the pathophysiological activities and processes of RNA NR2F1-AS1 in cancer cells. Methods: The contents of the present review were based on information obtained from PubMed. In the data search, “NR2F1-AS1” was chosen as the first keyword, whereas “cancer” was chosen as the second keyword. This review selected and summarized studies published between 2019-2021, concerning the biological functions and mechanisms of NR2F1-AS1 in the development of tumorigenesis. Results: It was found that NR2F1-AS1 regulates a variety of biological activities such as proliferation, invasion, migration, and apoptosis. It acts as an oncogene because it is abnormally expressed and promotes the progression of cancer in a variety of malignancies, including esophageal squamous cell carcinoma, non-small cell lung cancer, breast cancer, neuroblastoma, endometrial cancer, thyroid cancer, and gastric cancer. However, it was evident that NR2F1-AS1 inhibits the progression of cancer in cervical squamous cell carcinoma. Conclusion: NR2F1-AS1 is a potential new biomarker and therapeutic target for the treatment of different cancers.

Background: Experimental evidence has shown that lncRNA MALAT1 is related to proliferation ability, invasion and migration ability, autophagy ability, and chemoresistance in gastric cancer. Moreover, MALAT1 is related to metastasis and patient prognosis in gastric cancer. This review aims to reveal the biological functions and specific mechanisms of MALAT1 in gastric cancer. Methods: After a comprehensive and systematic search in PubMed, various molecular mechanisms of MALAT1 in mediating gastric carcinogenesis are collated and summarized. Results: MALAT1-mediated gastric cancer is involved in a variety of molecular mechanisms. For example, MALAT1 can enhance the proliferation ability of gastric cancer cells by inhibiting the expressions of miR-122, miR-1297, miR-22-3p, miR-202, etc. MALAT1 enhances the metastasis and invasion of gastric cancer by participating in the EMT process, PI3-Akt and other pathways. MALAT1 enhances the proliferation and invasion of gastric cancer by inhibiting the function of the tumor suppressor gene PCDH10. MALAT1 can increase the autophagy ability of gastric cancer cells by inhibiting miR-183 and increasing the level of autophagy markers. MALAT1 enhances chemical resistance by inhibiting UPF1 and miR-30e levels. Conclusions: MALAT1 is tightly linked to gastric carcinogenesis through various molecular mechanisms. Moreover, MALAT1 is also closely associated with chemoresistance and poor prognosis in gastric cancer patients, suggesting the possibility of its use as a clinical therapeutic target and a promising independent risk factor for predicting patient prognosis.

Background: It is substantiated that LncRNAs are associated with carcinoma progression. OIP5- AS1 is a tumor-related carcinoma suppressor lncRNA, previously discovered in zebrafish, which is involved in the progression of a variety of cancers, has a regulatory effect on carcinoma, and interacts with miRNA and other biomolecules to affect the physiological and pathological processes of carcinoma cells. This article will discuss the effect of OIP5-AS1 in various cancers and its regulatory mechanism. Methods: This paper summarized and analyzed OIP5-AS1, which functions on the germination and progression of carcinoma and its regulatory mechanism. Meanwhile, the related research was retrieved and collected by the PubMed system. Results: OIP5-AS1 is overexpressed in various tumors, which regulates and controls tumor growth and participates in tumor progression, including breast carcinoma, ovarian carcinoma, cervical carcinoma, lung carcinoma, laryngeal squamous cell gastric carcinoma and hepatocellular carcinoma. The research evidence proves that OIP5-AS1 takes part in carcinoma proliferation, growth, migration, invasion, and apoptosis. Conclusion: OIP5-AS1 probably can be an effective biomarker or a potential therapeutic target in multiple tumors.

Background: Long non-coding RNAs (lncRNAs) has no protein-coding potential due to the lack of an apparent open reading frame. There is growing evidence that lncRNA DGCR5 has a vital regulatory role in human illnesses' pathological development, particularly in the digestive system's carcinogenesis and progression. Abnormal DGCR5 expression affects different cellular functions such as proliferation, aggression, and metastasis. This paper aims to probe into the pathophysiological functions and molecular mechanisms of DGCR5 in cancers of the digestive system. Methods: This review summarizes and analyzes the biological functions and mechanisms of lncRNA DGCR5 in digestive system cancers occurrence. Relevant studies were conducted and reviewed by searching PubMed for articles with lncRNA DGCR5 and digestive system cancer as keywords in recent years. Results: DCGR5, as a novel tumor-related lncRNA, is recently identified to be abnormally expressed in digestive system cancers, such as pancreatic ductal adenocarcinoma, pancreatic cancer, gastric cancer, gallbladder cancer, colorectal cancer, and hepatocellular carcinoma. The role played by DCGR5 is vital and varies in different digestive cancers. Taken together, aberrant expression of DCGR5 regulates the progression of digestive cancers by affecting cancer cell proliferation, aggression, metastasis, and drug resistance. Conclusion: LncRNA DGCR5 might be a viable marker or a promising therapeutic target in digestive system cancers.

Background: Long noncoding RNA (lncRNA) fetal-lethal non-coding developmental regulatory RNA (FENDRR), a newly known lncRNA, has been reported to be abnormally expressed in diverse tumors. This review is focused on clarifying the mechanism of FENDRR to regulate the biological process of tumors, affirming its value as a target for tumor therapy. Methods: The pathophysiological mechanism of FENDRR acting on tumors has been analyzed and summarized by reviewing PubMed. Results: The expression of lncRNA FENDRR is abnormally altered in clinical cancers, promoting the malignant transformation of a variety of tumors, including colon cancer, cervical cancer, hepatocellular carcinoma, prostate cancer, Malignant melanoma, lung cancer, osteosarcoma, breast cancer, etc. Cellular processions, including proliferation, invasion, apoptosis and migration affected by FENDRR, have been revealed. Conclusion: Specific evidences for the involvement of LncRNA FENDRR in cancer regulatory processes suggest that FENDRR has the potential to be a biomarker or clinical therapeutic target for malignant tumors.

Background: Long non-coding RNA (lncRNA) with little or no coding ability has shown a variety of biological functions in cancer, including epigenetic regulation, DNA damage, regulation of microRNAs, and participation in signal transduction pathways. LncRNA can be used as an oncogene and tumor suppressor gene through transcriptional regulation in cancer. For example, the over-expressed lncRNA DLEU2 promotes the occurrence of laryngeal cancer, lung cancer, hepatocellular carcinoma, etc., and inhibits the progression of chronic lymphocytic leukemia. Deleted in Lymphocytic Leukemia 2 (DLEU2), as one of the long non-coding RNAs, was first found in chronic lymphoblastic leukemia and drawn into the progress of innumerable cancers. The molecular mechanism of DLEU2 in multiple tumors will be revealed. Methods: In this review, current studies on the biological functions and mechanisms of DLEU2 in tumors are summarized and analyzed; related researches are systematically retrieved and collected through PubMed. Results: DLEU2, a novel cancer-related lncRNA, has been demonstrated to be abnormally expressed in various malignant tumors, including leukemia, esophageal cancer, lung cancer, glioma, hepatocellular carcinoma, malignant pleural mesothelioma, bladder cancer, pancreatic cancer, pharynx and throat cancer, renal clear cell carcinoma, breast cancer, osteosarcoma. Besides, lncRNA DLEU2 has been shown to be involved in the process of proliferation, migration, invasion and inhibition of apoptosis of cancer cells. Conclusion: Due to the biological functions and mechanisms involved in DLEU2, it may represent an available biomarker or potential therapeutic target in a variety of malignant tumors.

Background: There is increasing evidence that lncRNA, a type of transcript that is over 200 nucleotides in length and may serve as oncogenes or suppressor genes, is implicated in the pathophysiology of human diseases. In particular, tumorigenesis and progress are closely correlated with its abnormal expression. In addition, it may become a promising target for many oncology biotherapies. Abnormal DLX6-AS1 expression affects different cellular processes such as proliferation, aggression and metastasis. This review aims to probe into the pathophysiological functions and molecular mechanisms of DLX6-AS1 in various cancers. Methods: By retrieving the literature, this review summarizes the biological function and mechanism of LncRNA DLX6-AS1 in tumor occurrence. Results: The lncRNA DLX6-AS1 is a new tumor-related RNA that has recently been found to be aberrantly expressed in diverse cancers, such as pancreatic cancer, osteosarcoma, non-small cell lung cancer, gastric carcinoma, glioma, hepatocellular cancer, colorectal carcinoma, renal carcinoma, esophageal squamous cell cancer, ovarian cancer, Ewing sarcoma, cervical cancer, breast cancer, thyroid cancer, neuroblastoma, pulmonary adenocarcinoma, nasopharyngeal carcinoma, squamous laryngeal cancer and bladder cancer, etc. Meanwhile, it is identified that DLX6-AS1 regulates the aggression, translocation and proliferation of diverse cancers. Conclusion: LncRNA DLX6-AS1 may be viable markers in tumors or a potential therapeutic target for multiple tumors.

Background: Long non-coding RNAs (LncRNAs), with the length of over 200 nucleotides, that originate from intergenic, antisense, or promoter-proximal regions, are a large family of RNAs that lack coding capacity. Emerging evidences illustrated that LncRNAs played significant roles in a variety of cellular functions and biological processes in profuse human diseases, especially in cancers. Cancer susceptibility candidate 9 (CASC9), as a member of the LncRNAs group, firstly found its oncogenic function in esophageal cancer. In the following recent studies, a growing amount of human malignancies are verified to be correlated with CASC9, most of which are derived from the squamous epithelium tissue. This present review attempts to highlight the latest insights into the expression, functional roles, and molecular mechanisms of CASC9 in different human malignancies. Methods: In this review, the latest findings related to the pathophysiological processes of CASC9 in human cancers were summarized and analyzed, and the associated studies collected in systematic retrieval of PubMed used lncRNA and CASA9 as keywords. Results: CASC9 expression is identified to be aberrantly elevated in a variety of malignancies. The over-expression of CASC9 has been suggested to accelerate cell proliferation, migration, cell growth and drug resistance of cancer cells, while depressing cell apoptosis, revealing its role as an oncogene. Moreover, the current review demonstrated CASC9 as closely related to the neoplastic transformation of squamous epithelial cells and squamous metaplasia in non-squamous epithelial tissues. Finally, we discuss the limitations and tremendous diagnostic/ therapeutic potential of CASC9 in various human cancers. Conclusion: Long non-coding RNA CASC9 likely serve as useful disease biomarkers or therapeutic targets which be effectively applied in the treatment of different kinds of cancers.

Background: CASC15, one of long non-coding RNA, is involved in the regulation of many tumor biological processes, and is expected to become a new biological therapeutic target. This paper aims to elucidate the pathophysiological function of CASC15 in various tumors. Methods: The relationship between CASC15 and tumors was analyzed by searching references, and summarized the specific pathophysiological mechanism of CASC15. Results: LncRNA CASC15 is closely related to tumor development, and has been shown to be abnormally high expressed in all kinds of tumors, including breast cancer, cervical cancer, lung cancer, hepatocellular carcinoma, gastric cancer, bladder cancer, colon cancer, colorectal cancer, cardiac hypertrophy, intrahepatic cholangiocarcinoma, leukemia, melanoma, tongue squamous cell carcinoma and nasopharyngeal carcinoma. However, CASC15 has been found to be down-expressed abnormally in ovarian cancer, glioma and neuroblastoma. Besides, it is identified that CASC15 can affect the proliferation, invasion and apoptosis of tumors. Conclusion: LncRNA CASC15 has the potential to become a new therapeutic target or marker for a variety of tumors.

Background: In view of the roles of long non-coding RNA CDKN2B antisense RNA 1 (CDKN2BAS1) in various human diseases, we investigated the function of CDKN2B-AS1 and explored its therapeutic and prognostic target value in multiple biological processes. The aim of this review was to explore the molecular mechanism and clinical significance of CDKN2B-AS1 in various types of diseases. Materials and Methods: In this review, the biological functions and mechanisms of lncRNA CDKN2B-AS1 in a variety of pathophysiological processes were summarized and analyzed. The correlated studies were collected via a systematic search of PubMed, Wiley Online Library, and ScienceDirect. Results: CDKN2B-AS1 is a potential long non-coding RNA that has been shown to be aberrantly expressed in various malignancies, containing hepatocellular carcinoma, intrahepatic cholangiocarcinoma, esophageal squamous cell carcinoma, gastric cancer, colonic adenocarcinoma, cervical cancer, ovarian cancer, breast cancer, glioma, lung cancer, laryngeal squamous cell carcinoma and osteosarcoma, involving in the processes of tumor cells proliferation, migration, invasion and inhibition of tumor cells apoptosis. Besides, CDKN2B-AS1 has been proved implicated in numerous non-malignant diseases, such as idiopathic pulmonary fibrosis, endometriosis, inflammatory bowel disease, intracranial aneurysm, diabetes mellitus and its complications, primary open angle glaucoma, ischemic stroke, atherosclerosis, coronary artery diseases, hypertension and heart failure, participating in the procession of lipid, carbohydrate metabolism and inflammation regulation. Conclusions: Long non-coding RNA CDKN2B-AS1 likely serves as a promising therapeutic target or prognosis biomarker in multiple human diseases.

Background: The change of lncRNA expression is known to affect the progression of tumors. This has fueled numerous investigations aiming at the mystery of lncRNA. Clear lncRNA has been the hotspot of antisense RNAs research. More and more lncRNAs have been proven to take effect as oncogenes of multitudinous cancers and accelerate tumor progression. This review elucidates the pathophysiological functions of lncRNA DLGAP1-AS1 and lncRNA DLGAP1-AS2 in a variety of tumors. Methods: Via systematic analysis and in-depth study about relevant articles in PubMed, this article analyzes and summarizes the mechanism of antisense transcripts DLGAP1- AS1 and DLGAP1-AS2 in tumor development. Results: DLGAP1-AS1 and DLGAP1-AS2 can exert their effect as oncogenes on various cancers. The expression of DLGAP1-AS1 is aberrantly high in various tumors, including GC, BC, HCC, glioblastoma and CRC. Concurrently, in LC, RC, HCC, GC, glioma and CCA, DLGAP1-AS2 is also discovered to be highly expressed. And they have a strong pertinence with a poor prognosis. The disorder of DLGAP1-AS1 and DLGAP1- AS2 in different tumors has different malignant impacts on tumors, not only to invasion, apoptosis, multiplication and EMT of tumor cells but also to drug resistance and radioresistance. In addition, DLGAP1-AS2 was revealed to have the ability to predict the prognosis of WT and RCC. Conclusion: The regulatory effects of DLGAP1-AS1 and DLGAP1-AS2 on tumors make them possible to be clinical markers for the early diagnosis of tumors and effective therapeutic targets.

Background: Abundant studies have shown that non-coding RNA is connected with tumor cell growth, migration and invasion. As a newly discovered non-coding RNA, WDFY3-AS2 has gradually emerged in the molecular mechanism of various tumors and has a potential prospect as a biological indicator of tumor prognosis. This review describes the pathophysiological mechanism and prognostic value of WDFY3-AS2 in different cancers. Objective: This review reveals the changes and roles of WDFY3-AS2 in many tumors and cancers. The change of WDFY3-AS2 can be used as a cancer biomarker and plays an important role in improving tumor growth, migration and invasion. WDFY3-AS2 is unique because it can be considered a prognostic marker for many tumors and is of great significance for clinical diagnosis and treatment. WDFY3-AS2 shows the potential prognostic value and the prospect of therapeutic targets in various tumors. Methods: PubMed reviewed the related literature to analyze and summarize the regulatory molecular mechanism of WDFY3-AS2 in various tumors and its value as a prognostic indicator. Results: The abnormal expression of LncRNA WDFY3-AS2 in many cancers was connected with the poor prognosis of cancer patients, including diffuse glioma, hepatocellular carcinoma, ovarian cancer, esophageal cancer, triple-negative breast cancer, Clear Cell Renal Carcinoma, Esophageal squamous cell carcinoma, Lung adenocarcinoma, which participated in the recovery of orthodontic teeth. WDFY3-AS2 has revealed the cellular process of cancer cell growth, migration, and invasion. Conclusion: The molecular mechanism of LncRNA WDFY3-AS2 regulating tumor specifically proves that WDFY3-AS2 has a good prospect in the biological index of prognosis or clinical treatment target of cancer patients.

Background: As a member of long non-coding RNAs (lncRNAs), maternally expressed gene 8 (MEG8) has been found involving in the progression of a variety of cancers and playing a regulatory role. Therefore, MEG8 may turn into a new therapeutic target for cancer in the future. The purpose of this review is to illustrate the molecular mechanism and physiological function of MEG8 in various cancers. Methods: We retrieved and analyzed related articles about MEG8, lncRNAs, and cancers, and then summarize the pathophysiological mechanisms of MEG8 in cancer development. Results: LncRNA MEG8 participates in various cancers progression, thus influencing the proliferation, migration, and invasion of cancers. However, the expression of MEG8 is abnormally upregulated in non-small cell lung cancer (NSCLC), pancreatic cancer (PC), liver cancer (HCC), pituitary adenoma (PA) and hemangioma (HA), and inhibited in colorectal cancer (CRC), ovarian cancer (OC) and giant cell tumor (GCT), suggesting its clinical value in cancer therapy. Conclusions: LncRNA MEG8 is expected to be a new therapeutic target or biomarker for a wide range of cancers in the future.

Background: More and more shreds of evidence show that the occurrence and development of tumors are closely related to the abnormal expression of LncRNA. A large number of experiments have found that overexpression or under-expression of MCM3AP-AS1 can affect the occurrence and development of cancer cells in varying degrees, such as proliferation, invasion, and translocation. Besides, MCM3AP-AS1 may become a promising target for many tumor biotherapies. This article reviews the pathophysiological functions and molecular mechanisms of MCM3AP-AS1 in various tumors. Methods: This paper systematically summarizes the published literatures in PubMed. The molecular mechanism of MCM3AP-AS1 in a variety of tumors is reviewed. Results: The abnormal expression of MCM3AP-AS1 in different tumors is closely related to tumor proliferation, invasion, and migration. MCM3AP-AS1 mediates or participates in related signaling pathways to regulate the expression of targeted miRNAs and proteins. MCM3AP-AS1 plays a vital role in tumor diagnosis and treatment. Conclusion: LncRNA MCM3AP-AS1 is a feasible tumor marker and a potential therapeutic target for many kinds of tumors.

Abstract: Integrins are a class of cell surface adhesion molecules composed of α subunit (ITGA) and β subunit (ITGB). They belong to heterodimer transmembrane glycoproteins. Their main function in organisms is as the receptor of cell adhesion molecules (CAMs) and extracellular matrix (ECM). According to the current research integration analysis, integrin α9 (ITGA9) is one of the integrin subunits, and there are few studies on ITGA9 among integrins. ITGA9 can improve cell migration and regulate various cellular biological functions, such as tumor cell proliferation, adhesion, invasion, and angiogenesis. However, its abnormal expression mechanism in cancer and its specific role in tumor growth and metastasis are still unknown to a great extent. This review reveals the role of ITGA9 in the complex pathogenesis of many tumors and cancers, providing a new direction for the treatment of tumors and cancers. Relevant studies were retrieved and collected through the PubMed system. After determining ITGA9 as the research object, we found a close relationship between ITGA9 and tumorigenesis by analyzing the research articles on ITGA9 in the PubMed system in the last 15 years and further determined the references mainly based on the influencing factors of the articles. Thus, the role of ITGA9 in tumor and cancer genesis, proliferation, and metastasis was reviewed and analyzed. ITGA9 is an integrin subunit, which has been proved to be abnormally expressed in many tumors. After sorting and analyzing the research data, it was found that the abnormal expression of ITGA9 in a variety of tumors, including glioblastoma, rhabdomyosarcoma, melanoma, hepatocellular carcinoma, nasopharyngeal carcinoma, multiple myeloma, non-small cell lung cancer, and prostate cancer, was closely related to the proliferation, metastasis, adhesion, and angiogenesis of tumor cells. These results suggest that ITGA9 plays an important role in the occurrence and development of tumors. The integrin subunit ITGA9 may serve as a biomarker for the diagnosis of tumors and a potential therapeutic target for anti-tumor therapies.

MicroRNAs (miRNAs) are an evolutionarily conserved class of small regulatory noncoding RNAs, binding to complementary target mRNAs and resulting in mRNA translational inhibition or degradation, and they play an important role in regulating many aspects of physiologic and pathologic processes in mammalian cells. Thus, efficient manipulations of miRNA functions may be exploited as promising therapeutics for human diseases. Two commonly used strategies to inhibit miRNA functions include direct transfection of chemically synthesized miRNA inhibitors and delivery of a gene vector that instructs intracellular transcription of miRNA inhibitors. While most miRNA inhibitors are based on antisense molecules to bind and sequester miRNAs from their natural targets, it is challenging to achieve effective and stable miRNA inhibition. Here we develop a user-friendly system to express circular inhibitors of miRNA (CimiRs) by exploiting the noncanonical head-to-tail backsplicing mechanism for generating endogenous circular RNA sponges. In our proof-of-principle experiments, we demonstrate that the circular forms of the hsa-miR223-binding site of human β-arrestin1 (ARRB1) 3′ UTR sponge RNA (BUTR), the bulged anti-miR223 (cirBulg223) and bulged anti-miR21 (cirBulg21), exhibit more potent suppression of miRNA functions than their linear counterparts. Therefore, the engineered CimiR expression system should be a valuable tool to target miRNAs for basic and translational research. Keywords: microRNA, miRNA, miRNA sponge, circular RNA, miRNA inhibitor, competing endogenous RNA, miRNA decoy, noncoding RNA, oncomiR

Background: Muscle blind-like-proteins (MBNL) are a class of tissue-specific RNA metabolism regulators that control pre-messenger RNA-splicing. Inactivation of MBNL can lead to myotonic dystrophy in adults. MBNL is mainly expressed in skeletal muscle, neuron tissue, thymus, liver, and kidney and plays an important role in the ultimate differentiation of muscle cells and neurons. MBNL1 is a member of the MBNL protein family. The inactivation of MBNL1 protein is particularly important in the development of myotonic dystrophy and can lead to cataract formation, abnormal muscle relaxation, cardiac and neurological dysfunction, etc. The induction of MBNL1 in tumors is known to significantly inhibit tumor progression and thus significantly prolong survival. MBNL1 antisense protein MBNL1-AS1 also plays an important role in tumor migration and development. Objective: This review reveals the role of MBNL1 and MBNL1-AS1 in the complex pathogenesis of many tumors, which provide a new target for the treatment of tumors. Methods: Correlated research are systematically retrieved via PubMed. In this review, the role of MBNL1 and MBNL1- AS1 were analyzed. Results: MBNL1 is down-regulated in breast cancer, leukemia, stomach cancer, esophageal cancer, glioma, and Huntington's disease. The function of inhibiting tumor cell metastasis decreased. It is up-regulated in cervical cancer and colorectal cancer, which can promote the development of tumor cells. Antisense protein MBNL1- AS1 can inhibit tumor cell proliferation and metastasis in colorectal cancer, non-small cell lung cancer, and gastric cancer. Conclusion: MBNL1 is an important regulator of tumor metastasis and growth, which exhibits a promising therapeutic target and can be further explored.

Background: Long non-coding RNA rhabdomyosarcoma 2-associated transcript (LncRNA RMST) can affect every aspect of tumor progressions, such as proliferation, translocation, and apoptosis. As a result, RMST can be used as an attractive biomarker for early diagnosis and clinical therapies of different disease states. This article aims to review pathophysiological functions, molecular mechanisms as well as promising biotherapies of RMST in multiple tumors. Methods: Through the systematic induction and summary of 46 papers published in PubMed concerning this study, the molecular mechanisms of RMST in all kinds of tumors have been reviewed. Results: LncRNA RMST is a tumor-related regulatory mediator, aberrantly expressed in diverse tumors, including medullary thyroid cancer, hepatocellular carcinoma, endometrial carcinoma, colon cancer, pancreatic cancer, glioma, Wilm’s tumor, and breast cancer. Furthermore, as a mechanismbased player, RMST probably guides the translation and post-translation modification, containing DNA methylation and SUMOylation. It is capable of regulating distinct tumor cells and stem cells of biological behaviors via various molecular pathways. Conclusion: LncRNA RMST, potentially as an original therapeutic target, is valuable in the occurrence, development, and apoptosis of different tumors.

Background: Long non-coding RNAs (lncRNA) have influenced numerous biology processes, which has provoked great interest. Not only that, LncRNA DUXAP8 mediates tumorigenesis by affecting the activity of miRNAs, signaling pathways, and oncogene. Methods: The functions of DUXAP8 have been summarized by reading relevant articles on PubMed. Results: lncRNA DUXAP8 acts as an oncogene in most tumors. The abnormal overexpression is associated with the proliferation, invasion, migration, and anti-autophagy of tumors. DUXAP8 exerts promotion on Akt / mTOR signaling pathway, facilitating the occurrence of tumors. Furthermore, DUXAP8 affects the activity of miRNAs and proteins, showing its significant potential as a therapeutic target in human cancers. Conclusion: LncRNA DUXAP8 has been identified as an indispensable therapeutic target of the tumors, providing clinical treatment plans.

Background: As it is known, long non-coding RNA (lncRNA) affects tumor progression, which has caused a great upsurge in recent years. It can also affect the growth, migration, and invasion of tumors. The abnormal expression of lncRNA is associated with malignant tumors. In addition, it has been proved that lncRNA is a key targeted gene for the treatment of some diseases. PART1, a member of lncRNA, has been reported as a regulator in the process of tumor occurrence and development. This study aims to reveal the biological functions, specific mechanisms, and clinical significance of PART1 in various tumor cells. Methods: Through the careful search of PUBMED, the mechanisms of the effect of PART1 on tumorigenesis and development are summarized. Results: On the one hand, the up-regulated expression of PART1 plays a tumor-promoting role in tumors, including lung cancer, prostate cancer, bladder cancer, and so on. On the other hand, PART1 is down-regulated in gastric cancer, glioma, and other tumors to play a tumor inhibitory role. In addition, PART1 regulates tumor growth mainly by targeting microRNA, such as miR-635, directly regulating the expression of proteins, such as FUS/EZH2, affecting signal pathways, such as Toll-like receptor pathway, or regulating immune cells. Conclusion: PART1 is closely related to tumors by regulating a variety of molecular mechanisms. In addition, PART1 can be used as a clinical marker for the early diagnosis of tumors and plays an important role in tumortargeted therapy.

Background: Long non-coding RNAs (lncRNA) have been identified as novel molecular regulators in cancers. LncRNA ADAMTS9-AS2 can mediate the occurrence and development of cancer through various ways, such as regulating miRNAs, activating the classical signaling pathways in cancer, and so on, which have been studied by many scholars. In this review, we summarize the molecular mechanisms of ADAMTS9-AS2 in different human cancers. Methods: Through a systematic search of PubMed, lncRNA ADAMTS9-AS2 mediated molecular mechanisms in cancer are summarized inductively. Results: ADAMTS9-AS2 aberrantly expression in different cancers is closely related to cancer proliferation, invasion, migration, and inhibition of apoptosis. The involvement of ADAMTS9-AS2 in DNA methylation, mediating PI3K / Akt / mTOR signaling pathways, and regulating miRNAs and proteins, shows its significant potential as a therapeutic cancer target. Conclusion: LncRNA ADAMTS9-AS2 can become a promising biomolecular marker and a therapeutic target for human cancer.

Background: Endometrial cancer is the fourth most common malignancy in female population worldwide. It was estimated that 65,620 new cases and 12.590 subsequent deaths occurred in 2020 in the United States. Patients with type II and advanced endometrial cancer do not respond well to the current treatments. Therefore, endometrial cancer should be better understood in order to develop more effective treatments. Objective: To provide an overview of genetic, metabolic characteristics, therapeutic strategies and current application of nanotechnology surrounding endometrial cancer. Method: Relevant articles were retrieved from Pubmed and were systematically reviewed. Results: Hypoxia inducible factor-1 and Von Hippel-Lindau factor participated in oncogenesis and progression of endometrial cancer and Nrf2 was associated with oncogenesis. Various genetic alterations were found in endometrial cancer. Examining the abnormal X chromosome inactivation may help in the diagnosis of endometrial cancer and its precancerous lesions. Some absent tumor suppressor genes, activated oncogenes were revealed by the genetically modified mouse models. Disorders in glucose and lipid metabolism were found in endometrial cancer. Current therapeutic strategies focused on the HIF-1α pathway, the mTOR pathway as well as the immunotherapy. Nanotechnology showed great potential in endometrial cancer’s early diagnosis, metastasis determination and treatment. Conclusion: Endometrial cancer has been understood in various aspects but the underlying mechanisms still remain relatively unknown, which might be the source of novel diagnostic, prognostic and therapeutic targets. Nanomedicine in endometrial cancer is poorly studied but the current researches showed great results in treating endometrial cancer. It needs further researching.

Background: Long non-coding RNA (lncRNA) breast cancer anti-estrogen resistance 4 (BCAR4) is a characterized oncogenic lncRNA in different cancers. This review is dedicated to summarize various molecular mechanisms of BCAR4 and demonstrate that the biological functions exerted by BCAR4 are good entry points for therapy. Methods: The molecular mechanism of BCAR4 acting on tumors is summarized by reviewing PubMed. Results: The expression of lncRNA BCAR4 is abnormally increased in all kinds of tumors, including colorectal cancer, prostate cancer, bladder cancer, gastric cancer, chondrosarcoma, glioma, breast cancer, glioma, gastric cancer, liver cancer, cervical cancer, lung cancer, etc. Besides, BCAR4 mediates multiple processes involved in carcinogenesis, including proliferation, invasion, anti-apoptosis, migration. Conclusion: BCAR4 may show great clinical value in this direction as a therapeutic cancer target.

Alkaloids are nitrogen-containing organic compounds widely found in natural products, which play an essential role in clinical treatment. Cellular signaling pathways in tumors are a series of enzymatic reaction pathways that convert extracellular signals into intracellular signals to produce biological effects. The ordered function of cell signaling pathways is essential for tumor cell proliferation, differentiation, and programmed death. This review describes the antitumor progression mediated by various alkaloids after inhibiting classical signaling pathways; related studies are systematically retrieved and collected through PubMed. We selected the four currently most popular pathways for discussion and introduced the molecular mechanisms mediated by alkaloids in different signaling pathways, including the NF-kB signaling pathway, PI3K/AKT signaling pathway, MAPK signaling pathway, and P53 signaling pathway. The research progress of alkaloids related to tumor signal transduction pathways and the realization of alkaloids as cancer prevention drugs by targeting signal pathways remains.

Background: LncRNA is a kind of non-coding RNA and its research is more popular in recent years, which has more than 200 nucleotides. It plays a significant part in various biological functions, including chromosome modification, genome modification, transcriptional activation, transcriptional interference, and other processes. FTX, at the center of the X chromosome inactivation and it has been shown that lncRNA FTX regulates cancer cells’ development, migration, and invasion in many studies. Methods: Relevant literatures were collected through PubMed system search and summarized. Results: LncRNA FTX abnormally increased in tumor cells, such as liver cancer, stomach cancer, leukemia, renal cell carcinoma, colorectal cancer, glioma, osteosarcoma, etc. However, the expression level decreased in temporal lobe epilepsy, liver cirrhosis, heart failure, etc. Conclusion: FTX may be an important regulatory factor and a potential therapeutic target in cancers.

Background: Osteoporosis (OP) is the most common bone disease, which is listed by the World Health Organization (WHO) as the third major threat to life and health among the elderly. The etiology of OP is multifactorial, and its potential regulatory mechanism remains unclear. Long non-coding RNAs (LncRNAs) are the non-coding RNAs that are over 200 bases in the chain length. Increasing evidence indicates that LncRNAs are the important regulators of osteogenic and adipogenic differentiation, and the occurrence of OP is greatly related to the dysregulation of the bone marrow mesenchymal stem cells (BMSCs) differentiation lineage. Meanwhile, LncRNAs affect the occurrence and development of OP by regulating OP-related biological processes. Methods: In the review, we summarized and analyzed the latest findings of LncRNAs in the pathogenesis, diagnosis and related biological processes of OP. Relevant studies published in the last five years were retrieved and selected from the PubMed database using the keywords of LncRNA and OP. Results/Conclusion: The present study aimed to examine the underlying mechanisms and biological roles of LncRNAs in OP, as well as osteogenic and adipogenic differentiation. Our results contributed to providing new clues for the epigenetic regulation of OP, making LncRNAs the new targets for OP therapy.

Background: In recent decades, the incidence of obesity has been rising globally. Obesity can often cause various inflammatory reactions, resulting in several diseases that threaten public health. The purpose of this review is to explore the role of long non-coding RNAs in metabolic obesity and find new targets for the prevention and treatment of metabolic diseases. Methods: We described the relationship between obesity and inflammation, reviewed several signaling pathways in metabolic inflammation, and summarized some of the long non-coding RNAs and their targets associated with metabolic inflammation. The related studies were retrieved through a systematic search of the PubMed database. Result: Metabolic stress during obesity can cause inflammation through several metabolic pathways. Many long non-coding RNAs can affect the progression of metabolic inflammation by affecting different pathways. Conclusion: Downregulation or antagonization of long non-coding RNAs in metabolic pathways may provide new ideas and therapeutic targets for the prevention and treatment of metabolic inflammation.

Background: Long non-coding RNAs (lncRNAs) with little or no coding capacity are associated with a plethora of cellular functions, participating in various biological processes. Cumulative study of lncRNA provides explanations to the physiological and pathological processes and new perspectives to the diagnosis, prevention, and treatment of some clinical diseases. Long non-coding RNA taurine-upregulated gene 1(TUG1) is one of the first identified lncRNAs associated with human disease, which actively involved in various physiological processes, including regulating genes at epigenetics, transcription, post-transcription, translation, and posttranslation. The aim of this review was to explore the molecular mechanism of TUG1 in various types of human diseases. Methods: In this review, we summarized and analyzed the latest findings related to the physiologic and pathophysiological processes of TUG1 in human diseases. The related studies were retrieved and selected the last six years of research articles in PubMed with lncRNA and TUG1 as keywords. Results: TUG1 is a valuable lncRNA that its dysregulated expression and regulating the biological processes were found in a variety of human diseases. TUG1 is found to exhibit aberrant expression in a variety of malignancies. Dysregulation of TUG1 has been shown to contribute to proliferation, migration, cell cycle changes, inhibited apoptosis, and drug resistance of cancer cells, which revealed an oncogenic role for this lncRNA, but some reports have shown downregulation of TUG1 in lung cancer samples compared with noncancerous samples. In addition, the molecular and biological functions of TUG1 in physiology and disease (relevant to endocrinology, metabolism, immunology, neurobiology) have also been highlighted. Finally, we discuss the limitations and tremendous diagnostic/therapeutic potential of TUG1 in cancer and other diseases. Conclusion: Long non-coding RNA-TUG1 likely served as useful disease biomarkers or therapy targets and effectively applied in different kinds of diseases, such as human cancer and cardiovascular diseases.

Background: Ovarian cancer is the most malignant tumor in gynecological tumors, with low five-year survival rate. The main reasons are diagnosis at advanced stages (the early symptoms are uncharacteristic, and most are diagnosedlate.), relapse, and resistance to existing chemotherapy drugs. Methods: Search strategy was performed in the following steps. Firstly, LncRNA related to ovarian cancer was retrieved by using the LncRNA Disease database, and articles were searched by searching keywords: ovarian cancer, drug resistance, and LncRNA retrieved from the LncRNA Disease database. Results/Conclusion: With the development of the study on drug resistance of ovarian cancer, the role of LncRNAs as sensitive biomarker and therapeutic target has emerged, providing a direction for precision medicine of ovarian cancer resistance.

We have previously reported that polysaccharides extracted from Pyracantha fortuneana (Maxim.) Li (P. fortuneana) lowered the oxidative stress and inhibited the inflammatory responses in mice. Our present study aims to determine the effects of Selenium enriched P. fortuneana polysaccharides (Se-PFPs) against carbon tetrachloride (CCl 4 )-induced liver injury in a mouse model. Our results displayed that CCl4 remarkably elevated the levels of alanine transferase (ALT), aspartate transaminase (AST), lactic dehydrogenase (LDH), cholesterol, triglycerides in serum. However, similar to BP treatment, supplementation of mice with Se-PFPs resulted in reversal of ALT, AST, LDH, cholesterol, triglycerides in serum. Contrary to CCl 4 , supplementation of mice with Se-PFPs elevated the activities of superoxide dismutase (SOD), glutathione peroxidase (GPx) and levels of glutathione (GSH) in liver. Furthermore, Se-PFPs treatment increased the expression of GPx and catalase (CAT) at mRNA and protein levels in liver which were decreased in CCl 4 group. Contrary to CCl 4 , Se-PFPs supplement decreased the levels of thiobarbituric acid reactive substances (TBAR) and H 2 O 2 , which served as lipid peroxidation biomarker. Our study indicates that Se-PFPs administration is effective in attenuating CCl 4 -induced liver injury. The mechanism underlying this effect may be attributed to the reduction of oxidative stress and inflammation in the liver by Se-PFPs through up-regulation of the antioxidant system. Our study suggests that Se-PFPs might be a potential dietary agent in the prevention of hepatic damage.

Both selenium (Se) and polysaccharides from Pyracantha fortuneana (Maxim.) Li (PFPs) (P. fortuneana) have been reported to possess antioxidative and immuno-protective activities. Whether or not Se-containing polysaccharides (Se-PFPs) have synergistic effect of Se and polysaccharides on enhancing the antioxidant and immune activities remains to be determined. We previously reported that polysaccharides isolated from Se-enriched P. fortuneana (Se-PFPs) possessed hepatoprotective effects. However, it is not clear whether or not they have anti-mutagenic effects. In the present study, we compared and evaluated anti-mutagenic effects of Se-PFPs at three concentrations (1.35, 2.7 and 5.4 g/kg body weight) with those of PFPs, Se alone or Se + PFPs in mice using micronucleus assay in bone marrow and peripheral blood as well as mitomycin C-induced chromosomal aberrations in mouse testicular cells. We also elucidated the underlying mechanism. Our results demonstrated that Se-PFPs inhibited cyclophosphamide (CP)-induced micronucleus formation in both bone marrow and peripheral blood, enhanced the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) in mouse liver, and reduced the activity and expression of cytochrome P450 1A (CYP4501A) in mouse liver in a dose-dependent manner. In addition, we found that the anti-mutagenic potential of Se-PFPs was higher than those of PFPs, Se alone or Se + PFPs at the same level. These results suggest that the anti-mutagenic potential of Se-PFPs may be mediated through the inhibition of the activity and expression of CYP4501A. This study indicates that application of Se-PFPs may provide an alternative strategy for cancer therapy by targeting CYP1A family.