期刊
CHINESE MEDICAL JOURNAL
卷 128, 期 7, 页码 941-947出版社
CHINESE MEDICAL ASSOC
DOI: 10.4103/0366-6999.154302
关键词
Cell Proliferation; Hepatocellular Carcinoma; MiR-27a; Peroxisome Proliferator-activated Receptor gamma
资金
- Frontier Interdiscipline Program of Norman Bethune Health Science Center of Jilin University [2013101001]
- Science and Technology Support Program of Jilin Province [3D512K903430]
- Young Scholars Program of Norman Bethune Health Science Center of Jilin University [2013201011]
- Nature Science Foundation of Jilin Province [201215079]
Background: MicroRNAs (miRNAs) function as essential posttranscriptional modulators of gene expression, and are involved in a wide range of physiologic and pathologic states, including cancer. Numerous miRNAs are deregulated in hepatocellular carcinoma (HCC). This study aimed to investigate the role of miR-27a in the development of HCC. Methods: The expression of MiR-27a was measured by quantitative real-time polymerase chain reaction (qRT-PCR). 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide was used to examine changes in the viability of HepG2, Bel-7402, Bel-7404 hepatoma cell lines associated with up-regulation or down-regulation of miR-27a. A dual-luciferase activity assay was used to verify a target gene of miR-27a. Immunohistochemistry, qRT-PCR, Western blotting analysis, and cell cycle and apoptosis flow cytometric assays were used to elucidate the mechanism by which miR-27a modulates liver cancer cell proliferation. Results: The expression of miR-27a was signi.cantly increased in HCC tissues and HepG2, Bel-7402, Bel-7404 hepatoma cell lines (P < 0.05). We also found that the down-regulation of miR-27a in HepG2 cells dramatically inhibited proliferation, blocked the G1 to S cell cycle transition and induced apoptosis (P < 0.05). In addition, miR-27a directly targeted the 3'-untranslated region of peroxisome proliferator-activated receptor gamma (PPAR-gamma), and ectopic miR-27a expression suppressed PPAR-gamma expression on the mRNA and protein levels. The rosiglitazone-induced overexpression of PPAR-gamma attenuated the effect of miR-27a in HCC cells. Conclusions: Our findings suggested that miRNA-27a promoted HCC cell proliferation by regulating PPAR-. expression. MiR-27a may provide a potential therapeutic strategy for HCC treatment.
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