These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: [Growth inhibition of human hepatocellular carcinoma by miRNA-204 via down-regulation of Bcl-2 and Sirt1 expression].
    Author: Li K, Xyu Q, Liu X, Liu Q, Wang M.
    Journal: Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi; 2015 Feb; 31(2):168-72. PubMed ID: 25652855.
    Abstract:
    OBJECTIVE: To investigate the level of microRNA-204 (miR-204) in human hepatocellular carcinoma (HCC) and its effect on the potential mechanism of tumorgenesis. METHODS: Real-time quantitative PCR (qRT-PCR) was applied to detect the expression of miR-204 in HCC (n=60) and the corresponding tumor-adjacent normal tissues. The expressions of Bcl-2 and Sirt1 were measured by immunohistochemistry (IHC). The artificial miR-204 was transiently transfected into human SMMC-7721 cells in vitro. The proliferation and apoptosis of the cells were detected by MTT assay and flow cytometry, respectively. The expression levels of Bcl-2 and Sirt1 mRNA and protein were determined by qRT-PCR and Western blotting, respectively. RESULTS: The expression level of miR-204 in HCC tissues was significantly lower than that in the adjacent normal tissues, and it was associated with tumor size, number of tumors and advanced TNM stage. The expressions of Bcl-2 and Sirt1 in the lower miR-204 level group were both higher than those in the higher miR-204 level group. Correlation analysis showed that miR-204 expression was negatively correlated with Bcl-2 and Sirt1 protein expression levels. Over-expressed miR-204 in SMMC-7721 cells suppressed cell proliferation and promoted cell apoptosis, and down-regulated mRNA and protein expressions of both Bcl-2 and Sirt1. CONCLUSION: The expression of miR-204 in HCC tissues was significantly lower than that in tumor-adjacent normal tissues. miR-204 could inhibit HCC cell proliferation and induce apoptosis by down-regulating the expressions of Bcl-2 and Sirt1.
    [Abstract] [Full Text] [Related] [New Search]