Sulforaphane inhibits TGF-β-induced epithelial-mesenchymal transition of hepatocellular carcinoma cells via the reactive oxygen species-dependent pathway

Wu,Jinsheng; Han,Jingli; Hou,Benxin; Deng,Chengwei; Wu,Huanliang; Shen,Liangfang

doi:10.3892/or.2016.4638

Sulforaphane inhibits TGF-β-induced epithelial-mesenchymal transition of hepatocellular carcinoma cells via the reactive oxygen species-dependent pathway

Authors:
- Jinsheng Wu
- Jingli Han
- Benxin Hou
- Chengwei Deng
- Huanliang Wu
- Liangfang Shen
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Affiliations: Department of Oncology, Nonkennada Hospital, Danzhou, Hainan, P.R. China, The Sixth Affiliated Hospital of Xinjiang Medical University, Xinjiang, P.R. China, Department of General Surgery, The Third People's Hospital of Hainan Province, Hainan, P.R. China, Department of Oncology, Xiangya Hospital, Central South University, Hunan, P.R. China
Published online on: February 26, 2016 https://doi.org/10.3892/or.2016.4638
Pages: 2977-2983

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Abstract

Sulforaphane is recognized as a safe antitumor agent derived from various cruciferous vegetables, including broccoli. It has been demonstrated that sulforaphase is a potent antitumor agent in diverse cancers. However, its effect on hepatocellular carcinoma remains largely unknown. Here, we show that sulforaphane inhibits TGF-β-induced epithelial-mesenchymal transition of hepatocellular carcinoma cell via the reactive oxygen species-dependent pathway. We found sulforaphane inhibited hepatocellular carcinoma cell proliferation in a dose- and time-dependent manner. Sulforaphane induced G0/G1 phase cell cycle arrest and promoted cell apoptosis. A set of experiments showed that sulforaphase inhibited hepatocellular carcinoma cell migration and invasion, inhibited the formation of fibroblast like mesenchymal cells and the expression of Vimentin, but increased the expression of E-cadherin, suggesting sulforaphane suppresses epithelial-mesenchymal transition (EMT) process. Cotreatment with N-acetyl-L-cysteine inhibited sulforaphane-inhibited invasion and upregulation of E-cadherin and almost completely abolished the sulforaphane-induced expression of Vimentin. The effect of sulforaphane on the growth of hepatocellular carcinoma cells was confirmed by a xenograft tumor growth model. All our finding indicated that sulforaphane is a promising and safe strategy for treating hepatocellular carcinoma.

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