期刊
INTERNATIONAL JOURNAL OF ONCOLOGY
卷 45, 期 4, 页码 1537-1546出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/ijo.2014.2577
关键词
miR-222; miRNA; sorafenib; hepatocellular carcinoma
类别
资金
- Development of Science and Technology Plan Projects of Jilin [209Z0198]
The miR-222 cluster has been demonstrated to function as oncomiR in human hepatocellular carcinoma (HCC). miR-222 confers chemotherapy drug resistance in various cancers, including HCC. However, the effects and mechanisms by which miR-222 regulates liver tumorigenicity and confers sorafenib (SOR) resistance remain unclear. Here we first investigated the miR-222 effect on proliferation, cell cycle, apoptosis, migration and invasion of HCC. Our results demonstrated that miRNA inhibitors specially targeting miR-222 significantly suppressed cellular proliferation, migration, invasion and G1/S transition of the cell cycle, and induced cell apoptosis in HepG2 cells. In addition, we investigated whether miR-222 confers SOR resistance in HepG2 cells to explore it roles in acquisition of drug resistance. The results showed that miR-222 inhibitors induced sensitivity to the antitumor effect of sorafenib in human HepG2 cells. Importantly, our study also showed that miR-222 could regulate the expression of phosphorylation PI3K and AKT, which might contribute to miR-222 conferred SOR resistance in HepG2 cells. In conclusion, this study demonstrates that miR-222 can promote cell proliferation, migration and invasion, and decrease cell apoptosis, as well as enhance the resistance of HCC cells to sorafenib miR-222 through activating the PI3K/AKT signaling pathway.
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