4.3 Article

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

Journal

ONCOTARGET
Volume 7, Issue 46, Pages 75749-75762

Publisher

IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.12407

Keywords

Alpha-fetoprotein; benzyl isothiocyanate (BITC); hepatocellular carcinoma; apoptosis

Funding

  1. National Natural Science Foundation of China [81660463, 81560450, 31560243, 81360307, 81260306, 81160261]
  2. Project of Hainan Province Innovative Team [2016CXTD008]
  3. Key Program of Science and Technology, Ministry of Education of China [211146]
  4. Key Projects of Science and Technology, Hainan Province [ZDXM 20110038]
  5. New Century Excellent Talents in China [NCET-10-0124]
  6. Natural Science Foundation of Hainan Province [309034, 310044, 811208, 814293, 20168263]
  7. Fund of Hainan Provincial Society Development [2015SF03]
  8. Hainan Provincial Association for Science and Technology Program of Youth Science Talent and Academic Innovation [201514]
  9. Hainan Provincial Department of Education [HjKj 2013-21]
  10. Undergraduate Student Innovate Project of Hainan Medical College [HYCX2014031, 20150067]

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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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