Abstract: Hepatocellular carcinoma is one of the most common and lethal cancers worldwide, especially in developing countries. In the present study, we found that the expression of a microRNA, miR-590-5P, was down-regulated and S100A10 was up-regulated in six hepatocellular carcinoma cell lines. The reporter gene assay showed that overexpression of miR-590-5P effectively reduced the activity of luciferase expressed by a vector bearing the 3' untranslated region of S100A10 mRNA. Ectopic miR-590-5P overexpression mediated by lentiviral infection decreased expression of S100A10. Infection of Lv-miR-590-5P inhibited cell growth and induced cell cycle G1 arrest in HepG2 cells. In addition, miR-590-5P expression suppressed the expression of Wnt5a, cMyc and cyclin D1, and increased the phosphorylation of β-catenin and expression of Caspase 3, which may contribute to the inhibitory effect of miR-590-5P on cell growth. Taken together, our data suggest that down-regulation of miR-590-5P is involved in hepatocellular carcinoma and the restoration of miR-590-5P can impair the growth of cancer cells, suggesting that miR-590-5P may be a potential target molecule for the therapy of hepatocellular carcinoma.
Keywords: miR-590-5P; S100A10; hepatocellular carcinoma; Wnt pathway; lentiviral system; reporter gene
Export to BibTeX
MDPI and ACS Style
Shan, X.; Miao, Y.; Fan, R.; Qian, H.; Chen, P.; Liu, H.; Yan, X.; Li, J.; Zhou, F. MiR-590-5P Inhibits Growth of HepG2 Cells via Decrease of S100A10 Expression and Inhibition of the Wnt Pathway. Int. J. Mol. Sci. 2013, 14, 8556-8569.
Shan X, Miao Y, Fan R, Qian H, Chen P, Liu H, Yan X, Li J, Zhou F. MiR-590-5P Inhibits Growth of HepG2 Cells via Decrease of S100A10 Expression and Inhibition of the Wnt Pathway. International Journal of Molecular Sciences. 2013; 14(4):8556-8569.
Shan, Xiangxiang; Miao, Yufeng; Fan, Rengen; Qian, Haixin; Chen, Ping; Liu, Hongqi; Yan, Xiaomei; Li, Jianping; Zhou, Fen. 2013. "MiR-590-5P Inhibits Growth of HepG2 Cells via Decrease of S100A10 Expression and Inhibition of the Wnt Pathway." Int. J. Mol. Sci. 14, no. 4: 8556-8569.