The morbidity and mortality of hepatocellular carcinoma (HCC) is very high, finding new therapeutic targets are critical for HCC treatment. miR-522 has been demonstrated to be upregulated in HCC tissues, but its role in HCC progression remains to be elucidated. In this report, we found miR-522 was upregulated in HCC cells and tissues, miR-522 overexpression promoted cell proliferation, colony formation, and cell cycle progression, whereas knockdown of miR-522 reduced these effects. We also analyzed the expression of several key cell cycle regulatory proteins and found overexpression of miR-522-inhibited cell cycle inhibitors p21 and p27 expression and enhanced cyclin D1 expression and the level of Rb phosphorylation, vice versa. These suggested miR-522-accelerated G1/S transition. DKK1 (dickkopf-1) and SFRP2 (secreted frizzled-related protein 2) were the targets of miR-522, their expression was inversely with miR-522 in HCC tissues. DKK1 and SFRP2 the antagonists of Wnt signaling, suggesting miR-522-promoted HCC progression through activating Wnt signaling. miR-522 might be a valuable target for HCC therapy.
Keywords: Cell proliferation; DKK1 and SFRP2; HCC; miR-522.