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MiR-1297 promotes cell proliferation by inhibiting RB1 in liver cancer.

ABSTRACT: Liver cancer is the one of the most common causes of cancer-associated mortality worldwide. MicroRNAs (miRNAs or miRs) are important in various types of cancer, including liver cancer. In the present study, with miRNA expression profile data obtained from the Gene Expression Omnibus database, three independent methods were used to investigate the miRNAs that are involved in liver carcinogenesis, including Fisher's exact test, t-test and Wilcoxon test. Five differentially expressed miRNAs were identified. Among them, miR-1297 drew specific attention. Target gene analysis and Ingenuity Pathway Analysis revealed its potential impact on cell death and cell cycle. Cell Counting Kit-8 proliferation assay indicated that the HepG2 cell proliferation was promoted by miR-1297, while miR-1297 inhibitor could significantly inhibit the proliferation of HepG2 cells. Luciferase assays confirmed that miR-1297 directly bound to the 3'-untranslated region of retinoblastoma (RB)1, and western blotting demonstrated that miR-1297 suppressed the expression of RB1 at the protein level. RB1 is involved in the regulation of the human cell cycle pathway. It is possible that miR-1297 contributes to the carcinogenesis of liver cancer via downregulation of the tumor-suppressor gene RB1. Our results suggest that miR-1297 may serve as a potential therapeutic target of liver cancer.

SUBMITTER: Liu C

PROVIDER: S-EPMC5228426 | biostudies-literature | 2016 Dec

REPOSITORIES: biostudies-literature

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miR-1297 promotes cell proliferation by inhibiting RB1 in liver cancer.

Liu Chengyong C Wang Chunying C Wang Ji J Huang Haibin H

Oncology letters 20161031 6

Liver cancer is the one of the most common causes of cancer-associated mortality worldwide. MicroRNAs (miRNAs or miRs) are important in various types of cancer, including liver cancer. In the present study, with miRNA expression profile data obtained from the Gene Expression Omnibus database, three independent methods were used to investigate the miRNAs that are involved in liver carcinogenesis, including Fisher's exact test, <i>t</i>-test and Wilcoxon test. Five differentially expressed miRNAs ...[more]

PMID: 28105225

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Project description:Background: Secreted protein acidic and rich in cysteine (SPARC) plays an important role in cancer development. The roles of SPARC in the liver hepatocellular carcinoma (LIHC) are unclear. Methods: GEPIA2 and UALCAN were used to analyze the SPARC mRNA expression levels in LIHC based on the TCGA database. The GEO database was used to verify the analysis results. Immunohistochemical (IHC) analysis was used to investigate the SPARC protein levels in LIHC tissues. The Kaplan-Meier (KM) plotter was used to analyze the correlation between SPARC and prognosis. The serum SPARC levels were measured by ELISA. CCK8 and murine xenograft models were used to investigate the effect of SPARC on the liver cancer growth in vitro and in vivo. SPARC-correlated genes were screened by LinkedOmics. Results: Based on the TCGA and GEO databases, the analysis showed that the SPARC mRNA expression levels were increased in tumor tissues and peripheral blood mononuclear cell (PBMC) from LIHC compared to normal controls. The IHC analysis showed an increased level of SPARC in LIHC tissues compared to adjacent non-tumor tissues. However, we found that the serum SPARC levels were lower in LIHC than those in healthy controls. The KM plotter showed that there was no significant correlation between the SPARC mRNA levels and overall survival. However, in sorafenib-treated LIHC patients, the high SPARC expression predicts favorable prognosis. Furthermore, the endogenous SPARC overexpression promotes liver cancer cell proliferation in vitro and tumor growth in vivo, while there was no significant effect of exogenous SPARC treatment on liver cancer cell proliferation. Function enrichment analysis of SPARC-correlated genes indicated a critical role of interaction with an extracellular matrix in SPARC-promoting cancer cell proliferation. Conclusion: SPARC mRNAs were increased in LIHC tumor tissues, and SPARC overexpression may promote the liver cancer growth. Further studies are needed to clarify the potential prognostic value of SPARC, both in tissues and in circulation.

Project description:The purpose of our study is to elucidate the expression of lncRNA00518 (lnc00518) in the bladder cancer, and its potential mechanism in regulating the development of bladder cancer. The expression of lnc00518 in bladder cancer tissues and cells was examined by qRT-PCR. Correlation between lnc00518 expression with clinicopathologic characteristics and prognosis of bladder cancer patients was analyzed. In vitro effects of lnc00518 on the cellular behaviors of bladder cancer cells were explored. Moreover, in vivo effect of lnc00518 was evaluated by subcutaneous tumorigenesis in nude mice. The possible miRNA targets of lnc00518 were predicted by bioinformatics and further confirmed by dual-luciferase reporter gene assay, RIP and rescue experiments. Lnc00518 was highly expressed in bladder cancer tissues and cells. Lnc00518 expression was correlated with TNM staging and histological grade of bladder cancer. Besides, the overall survival was lower in bladder cancer patients with high expression of lnc00518 relative to those with low expression. Overexpression of lnc00518 enhanced proliferative, invasive, migratory potentials and clonality, but shortened G0/G1 phase of bladder cancer cells. Lnc00518 knockdown obtained the opposite trends. In vivo experiments revealed that lnc00518 knockdown inhibited subcutaneous tumorigenesis in nude mice. QRT-PCR results indicated that lnc00518 expression was negatively correlated with miRNA-101 expression in bladder cancer cells. Through dual-luciferase reporter gene assay and RIP, we confirmed the binding between lnc00518 and miRNA-101. Furthermore, EZH2 was verified to be the target of miRNA-101. MiRNA-101 knockdown reversed the inhibitory roles of lnc00518 knockdown in proliferative, migratory and invasive potentials of bladder cancer cells. Lnc00518 is highly expressed in bladder cancer and can be served as a predictor of poor prognosis. Lnc00518 promotes the proliferative, invasive and migratory potentials of bladder cancer by upregulating EZH2 via competitively binding to miRNA-101.

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MiR-1297 promotes cell proliferation by inhibiting RB1 in liver cancer.

Publications

miR-1297 promotes cell proliferation by inhibiting RB1 in liver cancer.

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