SNAI 1 promotes the development of HCC through the enhancement of proliferation and inhibition of apoptosis

SNAI 1, a zinc‐finger transcription factor, plays an important role in the induction of epithelial–mesenchymal transition ( EMT ) in various cancers. However, the possible functions of SNAI 1 in the proliferation and apoptosis of hepatocellular carcinoma have not been clearly identified. In this study, we investigated the effects and mechanisms of SNAI 1 in the proliferation and apoptosis of hepatocellular carcinoma using clinical samples and cell lines. We found that SNAI 1 is highly expressed in the tissues of liver cancer compared with adjacent nontumor tissues. SNAI 1 is also highly expressed in the hepatoma cell lines HepG2, SMMC ‐7721, and BEL ‐7402 compared with the human normal liver cell line L02. We also observed that SNAI 1 expression was correlated with distal metastasis, incomplete tumor capsule formation, and histological differentiation in hepatocellular carcinoma ( HCC ). Moreover, we demonstrated that knockdown of SNAI 1 via lentiviral vectors of RNA i against SNAI inhibited cell proliferation by inducing G1 arrest, which was accompanied by the downregulation of cyclin D1 but not that of cyclin A. In addition, knockdown of SNAI 1 promoted apoptosis by decreasing the expression of Bcl‐2. In conclusion, our findings revealed that SNAI 1 is involved in the development of hepatocellular carcinoma via regulating the growth and apoptosis of tumor cells.