Study on the effect of microRNA-200a on the progression of hepatocellular carcinoma and the therapeutic effect of sorafenib

Acta Universitatis Medicinalis Anhui 2021 12 v.56 1860-1865     font:big middle small

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Authors:Wei Sheng; Zhou Dachen; Fang Chao; Yang Minghao; Zhao Huiyong; Pang Xiaoxi; Cui Xiao

Keywords:miR200a;hepatocellular carcinoma;sorafenib;SIRT1

DOI:10.19405/j.cnki.issn1000-1492.2021.12.003

〔Abstract〕 Objective To study the effect of microRNA-200 a(miR200 a) on the progression of hepatocellular carcinoma and the therapeutic effect of sorafenib. Methods The stable transformation cell lines of human hepatocellular carcinoma miR200 a were constructed: miR200 a overexpression, Control and miR200 a knockdown. The expression of miR200 a in each transfected cell line was detected by qRT-PCR, the expression of protein was detected by Western blot method, the cell′s vitality was detected by MTT method, and the ability of cell migration and invasion was detected by transwell method. After adding sorafenib to the transfected cell line, the effect of miR200 a on the regulation of sorafenib on cells and the changes of cell vitality and corresponding protein expression were detected by MTT and Western blot. Eighteen SPF male BALB/c-nu mice were randomly divided into 3 groups, with 6 mice in each group. miR200 a overexpression, Control and miR200 a knockdown cells were subcutaneously implanted in each group. After tumor formation, each group of nude mice were injected with sorafenib every day for 14 days. The nude mice were killed and the tumor volume was calculated. The expression and localization of tumor target protein were verified by immunohistochemistry. Results miR200 a could inhibit the cell viability and migration ability of hepatocellular carcinoma cells, and reduce the expression of SIRT1 at the same time. MiR200 a significantly reduced the tumor volume of nude mice. Conclusion miR200 a can inhibit the proliferation and migration of human hepatocellular carcinoma cell line and increase the efficacy of sorafenib, which may be achieved by regulating the expression of SIRT1.