Abstract:Long non-coding RNAs (lncRNAs) have been widely reported to regulate the development and chemoresistance of a variety of tumors. Temozolomide (TMZ) is a first-line chemotherapy for treatment of glioma. However, the effect and the regulatory mechanism of lncRNA MSC-AS1 (MSC-AS1) in TMZ-resistant glioma remain unrevealed. Levels of MSC-AS1, microRNA-373-3p (miR-373-3p), and cytoplasmic polyadenylation element binding protein 4 (CPEB4) were determined by quantitative real-time polymerase chain reaction (qRT-PCR).… Show more
“…MSC-AS1 was found to regulate the tumor progression by inhibiting miR-124 expression to increase CDK6 expression in osteosarcoma [ 21 ]. Moreover, MSC-AS1 acted as a role of carcinogenic factor in glioma by sponging miR-373-3p and upregulating CPEB4 [ 22 ]. Li et al reported that the expression of miR-325 was reduced in CRC [ 23 ].…”
Background. LncRNA MSC-AS1 has been reported to be a tumor promoter in hepatocellular carcinoma. However, the function of MSC-AS1 in colorectal cancer (CRC) has not been elucidated. It is designed to study the expression level of MSC-AS1 and investigate its biological effect on the progression of CRC. Methods. The expression patterns of MSC-AS1, miR-325, and TRIM14 were explored by RT-qPCR in CRC tissues and cells. The protein expression of TRIM14 was tested by Western blot assay. The association between MSC-AS1 expression and clinicopathological data was analyzed by chi-squared test. CCK-8 assay, colony formation, and Transwell assay were used to investigate the effect of MSC-AS1 on cell growth, invasion, and migration in CRC cells. The correlations among MSC-AS1, miR-325, and TRIM14 were analyzed by Pearson’s correlation coefficient analysis. Results. We found that MSC-AS1 and TRIM14 were upregulated in CRC tissues, while miR-325 was downregulated in CRC tissues. Functional experiments demonstrated that MSC-AS1 knockdown inhibited cell proliferation, migration, and invasion abilities in CRC cells. Additionally, miR-325 was proved to be a target miRNA of MSC-AS1, and TRIM14 might be a downstream gene of miR-325. Besides that, MSC-AS1 counteracted the inhibitory effect of miR-325 on the cell progression and TRIM14 expression. Conclusion. Our results indicated that MSC-AS1 facilitated CRC progression by sponging miR-325 to upregulate TRIM14 expression. We suggested that MSC-AS1 might be a potential lncRNA-target for CRC therapy.
“…MSC-AS1 was found to regulate the tumor progression by inhibiting miR-124 expression to increase CDK6 expression in osteosarcoma [ 21 ]. Moreover, MSC-AS1 acted as a role of carcinogenic factor in glioma by sponging miR-373-3p and upregulating CPEB4 [ 22 ]. Li et al reported that the expression of miR-325 was reduced in CRC [ 23 ].…”
Background. LncRNA MSC-AS1 has been reported to be a tumor promoter in hepatocellular carcinoma. However, the function of MSC-AS1 in colorectal cancer (CRC) has not been elucidated. It is designed to study the expression level of MSC-AS1 and investigate its biological effect on the progression of CRC. Methods. The expression patterns of MSC-AS1, miR-325, and TRIM14 were explored by RT-qPCR in CRC tissues and cells. The protein expression of TRIM14 was tested by Western blot assay. The association between MSC-AS1 expression and clinicopathological data was analyzed by chi-squared test. CCK-8 assay, colony formation, and Transwell assay were used to investigate the effect of MSC-AS1 on cell growth, invasion, and migration in CRC cells. The correlations among MSC-AS1, miR-325, and TRIM14 were analyzed by Pearson’s correlation coefficient analysis. Results. We found that MSC-AS1 and TRIM14 were upregulated in CRC tissues, while miR-325 was downregulated in CRC tissues. Functional experiments demonstrated that MSC-AS1 knockdown inhibited cell proliferation, migration, and invasion abilities in CRC cells. Additionally, miR-325 was proved to be a target miRNA of MSC-AS1, and TRIM14 might be a downstream gene of miR-325. Besides that, MSC-AS1 counteracted the inhibitory effect of miR-325 on the cell progression and TRIM14 expression. Conclusion. Our results indicated that MSC-AS1 facilitated CRC progression by sponging miR-325 to upregulate TRIM14 expression. We suggested that MSC-AS1 might be a potential lncRNA-target for CRC therapy.
“…As mentioned above, our KEGG pathway analysis suggested that the differentially expressed lncRNAs may regulate DV development via the PI3K/Akt pathway. Coincidentally, dysregulation of MSC-AS1 expression was found to promote tumor progression in glioma and osteosarcoma through the PI3K-Akt pathway [ 32 , 33 ], which may further support the important role of MSC-AS1/PI3K-Akt pathway in DV to a certain extent.…”
Long non-coding RNAs (lncRNAs) were considered to be involved in vascular complications in diabetes mellitus, but still only limited knowledge in this regard has been obtained. Herein, we further explored the roles of lncRNAs and mRNAs in diabetic vasculopathy (DV) through conducting bioinformatics analysis using data set downloaded from GEO database. The differentially expressed lncRNAs and mRNAs were identified by edge package. GO enrichment analysis and KEGG pathway analysis were performed based on clusterprofiler package. The relationship between lncRNA and miRNA was predicted using starBase database, and the potential mRNAs targeted by miRNAs were predicted by TargetScan, miRTarbase and miRDB database. The string database was used to analyze the protein-protein interaction (PPI). As a result, a total of 12 lncRNAs and 711 mRNAs were found to be differentially expressed in the diabetic subdermal endothelial cells compared with normal controls. A ceRNA network was established, which was composed of seven lncRNA nodes, 49 miRNA nodes, 58 mRNA nodes and 183 edges, and MSC-AS1 and LINC01550 may serve as key nodes. GO function enrichment analysis showed enrichments of epithelial cell proliferation, intercellular junction, and cell adhesion molecule binding. KEGG pathway analysis revealed 33 enriched pathways. PPI protein interaction analysis identified 57 potential ceRNA-related proteins. Overall, this study suggests that multiple lncRNAs, specifically MSC-AS1 and LINC01550, may play an important role in DV development and they are like to be developed as the therapeutic targets for DV. However, further experiments in vitro and in vivo should be conducted to validate our results.
“…MSC-AS1 induces PGK1 expression and accelerates the progression of HCC ( 30 ). In addition, MSC-AS1 has a similar role in gliomas ( 31 ), gastric cancer ( 32 ), renal clear cell carcinoma ( 33 ), and pancreatic cancer ( 34 ). TMEM220-AS1, AC015908.3, AC009005.1, and AL031985.3 have been reported in a signature predictive of overall survival.…”
BackgroundHepatocellular carcinoma is one of the most common malignant tumors with a very high mortality rate. The emergence of immunotherapy has brought hope for the cure of hepatocellular carcinoma. Only a small number of patients respond to immune checkpoint inhibitors, and ferroptosis and tertiary lymphoid structure contribute to the increased response rate of immune checkpoint inhibitors; thus, we first need to identify those who are sensitive to immunotherapy and then develop different methods to improve sensitivity for different groups.MethodsThe sequencing data of hepatocellular carcinoma from The Cancer Genome Atlas and Gene Expression Omnibus was downloaded to identify the immune-related long non-coding RNAs (lncRNAs). LncRNAs related to survival data were screened out, and a risk signature was established using Cox proportional hazard regression model. R software was used to calculate the riskScore of each patient, and the patients were divided into high- and low-risk groups. The prognostic value of riskScore and its application in clinical chemotherapeutic drugs were confirmed. The relationship between riskScore and immune checkpoint genes, ferroptosis genes, and genes related to tertiary lymphoid structure formation was analyzed by Spearman method. TIMER, CIBERSORT, ssGSEA, and ImmuCellAI were used to evaluate the relative number of lymphocytes in tumor. The Wilcoxon signed-rank test confirmed differences in immunophenoscore between the high- and low-risk groups.ResultsData analysis revealed that our signature could well predict the 1-, 2-, 3-, and 5-year survival rates of hepatocellular carcinoma and to predict susceptible populations with Sorafenib. The risk signature were significantly correlated with immune checkpoint genes, ferroptosis genes, and tertiary lymphoid structure-forming genes, and predicted tumor-infiltrating lymphocyte status. There was a significant difference in IPS scores between the low-risk group and the high-risk group, while the low-risk group had higher scores.ConclusionThe riskScore obtained from an immune-related lncRNA signature could successfully predict the survival time and reflect the efficacy of immune checkpoint inhibitors. More importantly, it is possible to select different treatments for different hepatocellular carcinoma patients that increase the response rate of immune checkpoint inhibitors and will help improve the individualized treatment of hepatocellular carcinoma.
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