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SNAI 1 promotes the development of HCC through the enhancement of proliferation and inhibition of apoptosis
Author(s) -
Qi Jianni,
Li Tao,
Bian Hongjun,
Li Feifei,
Ju Ying,
Gao Shanshan,
Su Jingran,
Ren Wanhua,
Qin Chengyong
Publication year - 2016
Publication title -
febs open bio
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.718
H-Index - 31
ISSN - 2211-5463
DOI - 10.1002/2211-5463.12043
Subject(s) - gene knockdown , apoptosis , cancer research , cell growth , cyclin d1 , hepatocellular carcinoma , downregulation and upregulation , cell culture , chemistry , metastasis , biology , cell cycle , cancer , gene , biochemistry , genetics
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.

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