miR-22-3p suppresses cell proliferation by regulating SP1 in hepatocellular carcinoma

Objective: Accumulating evidence has shown that microRNAs are involved in multiple processes in cancer development and progression. miR-22-3p was a widely studied regulator which has important roles in various kinds of cancers. While, the roles and specific mechanism of miR-22-3p in HCC development are not well understood. The aim of this study was to verify miR-22-3p expression level and its roles in proliferation, cell cycle and apoptosis inHCC cell lines. To investigate the potential mechanism of how miR-22-3p works in HCC progression. Methods: RT-PCR was used to detect the expression of miR-22-3p in one normal andfour HCC cell lines. Mimics or inhibitors were used for transfecting miR-22-3p. Small interfering RNA was applied to knockdown SP1 gene expression. Cell proliferation was conducted by MTT. Cell cycle and apoptosis assays were detectedusing flowcytometry. Western blot was used to detect the proteins expression level. Results: miR-22-3p expression was much lower than normal control (P<0.01). Transfection of miR-22-3p by mimics could significantly inhibits the cellar proliferation, increases the G0/G1 phase cells and induces apoptosis in HCC cell lines. miR-22-3p negatively regulated SP1, CCND1 and bcl2 expressionin HCC cell lines. Knockdown SP1 by siRNA inhibited the expression of CCND1 and bcl2, which is consistent with the miR-22-3p mimics group. Conclusion: miR-22-3p can act as a tumor suppressor in HCC. It may inhibit HCC cell proliferation through up-regulating SP1 and its downstream CCDN1 and bcl2 expression. These findings will contribute to the current understanding of miR-22-3p in HCC.