Background: Hepatocellular carcinoma (HCC) is one of the most common malignant tumors in human worldwide. Evidence indicated that upregulation of microRNA-3651 (miR-3651) was observed in human HCC tissues. In this study, we explored the mechanisms by which miR-3651 regulated the proliferation, apoptosis and invasion of HCC.
Methods: The levels of miR-3651 in human HCC tissues were detected using qRT-PCR assay. In addition, transwell invasion and Western blot assay were conducted to detect cell invasion and apoptosis, respectively. Meanwhile, the dual-luciferase reporter assay was used to explore the interaction of miR-3651 and phosphate and tension homology deleted on chromsome ten (PTEN) in HCC.
Results: The levels of miR-3651 were upregulated in HCC tissues in comparison with the matched normal tissues. Overexpression of miR-3651 significantly promoted the proliferation and invasion of Huh-7 cells. In contrast, inhibition of miR-3651 markedly inhibited the proliferation and invasion of Huh-7 cells via promoting apoptosis. Moreover, downregulation of miR-3651 markedly inhibited tumor growth in vivo. Furthermore, bioinformatics analysis and luciferase reporter assay identified that PTEN was the directly binding target of miR-3651 in Huh-7 cells. Meanwhile, overexpression of miR-3651 obviously decreased the level of PTEN, and increased the expressions of p-p85 and p-Akt in Huh-7 cells.
Conclusion: These results indicated that miR-3651 might act as a potential oncogene in HCC by targeting PTEN. Therefore, miR-3651 might be a novel therapeutic target for the treatment of HCC.
Keywords: hepatocellular carcinoma, microRNA-3651, PTEN, apoptosis