Research Papers:

Alpha fetoprotein antagonises benzyl isothiocyanate inhibition of the malignant behaviors of hepatocellular carcinoma cells

Mingyue Zhu, Wei Li, Junli Guo, Yan Lu, Xu Dong, Bo Lin, Yi Chen, Xueer Zhang and Mengsen Li _

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Oncotarget. 2016; 7:75749-75762. https://doi.org/10.18632/oncotarget.12407

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Mingyue Zhu1,2,*, Wei Li1,2,*, Junli Guo1, Yan Lu1,2, Xu Dong1,2, Bo Lin1,2, Yi Chen1,2, Xueer Zhang1,4, Mengsen Li1,2,3

1Hainan Provincial Key Laboratory of Carcinogenesis and Intervention, Hainan Medical College, Haikou 571199, Hainan Province, P.R. China

2Key Laboratory of Molecular Biology, Hainan Medical College, Haikou 571199, P.R. China

3Institution of Tumour, Hainan Medical College, Haikou 570102, Hainan Province, P.R. China

4Undergraduate Student of Clinical Medicine, Hainan Medical College, Haikou 571199, P.R. China

*These authors contribute equally to this work and are the co-first authors

Correspondence to:

Mengsen Li, email: [email protected]

Keywords: alpha-fetoprotein, benzyl isothiocyanate (BITC), hepatocellular carcinoma, apoptosis

Received: May 27, 2016    Accepted: September 20, 2016    Published: October 03, 2016


Benzyl isothiocyanate (BITC) is a dietary isothiocyanate derived from cruciferous vegetables. Recent studies showed that BITC inhibited the growth of many cancer cells, including hepatocellular carcinoma (HCC) cells. Alpha-fetoprotein (AFP) is a important molecule for promoting progression of HCC, in the present investigation, we explore the influence of AFP on the role of BITC in the malignant behaviours of HCC cells, and the potential underlying mechanisms. We found thatBITC inhibited viability, migration, invasion and induced apoptosis of human liver cancer cell lines, Bel 7402(AFP producer) and HLE(non-AFP producer) cells in vitro. The role of BITC involve in promoting actived-caspase-3 and PARP-1 expression, and enhancing caspase-3 activity but decreasing MMP-2/9, survivin and CXCR4 expression. AFP antagonized the effect of BITC. This study suggests that BITC induced significant reductions in the viability of HCC cell lines. BITC may activate caspase-3 signal and inhibit the expression of growth- and metastasis-related proteins; AFP is an pivotal molecule for the HCC chemo-resistance of BITC.

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