270P - Benzyl-isothiocyanate induces apoptosis and inhibits migration and invasion of hepatocellular carcinoma cells in vitro

Date 17 December 2016
Event ESMO Asia 2016 Congress
Session Poster lunch
Topics Basic Science
Hepatobiliary Cancers
Presenter Mengsen Li
Citation Annals of Oncology (2016) 27 (suppl_9): ix68-ix85. 10.1093/annonc/mdw582
Authors M. Li, M. Zhu, W. Li, J. Guo
  • Hainan Provincial Key Laboratory Of Carcinogenesis And Intervention, Hainan Medical College, 571199 - Hainan/CN

Abstract

Background

Despite consideration of benzyl isothiocyanate(BITC) is applied to prevention and therapeutic of cancer, the role of BITC in inducing apoptosis and inhibiting migration and invasion of hepatocellular carcinoma (HCC) cell is still unclear. In this study, we aims to explore the effects of BITC on the growth and migration and invasion of HCC cells in vitro.Despite consideration of benzyl isothiocyanate(BITC) is applied to prevention and therapeutic of cancer, the role of BITC in inducing apoptosis and inhibiting migration and invasion of hepatocellular carcinoma (HCC) cell is still unclear. In this study, we aims to explore the effects of BITC on the growth and migration and invasion of HCC cells in vitro.

Methods

Human HCC cell lines, Bel 7402 and HLE, were treated with an optimal concentration of BITC for 48 hours, and the growth and apoptosis of HCC cells were detected using the MTT method, fluorescent microscopy and flow cytometry. The migratory and invasive abilities of HCC cells were detected by Transwell assay, the MMP2 and MMP9 enzymatic activities were assayed by gelatin zymography, and the expression of apoptosis-related proteins and metastasis-related proteins was detected by Western blotting.

Results

MTT, fluorescent microscopy and flow cytometry analyses indicated that BITC inhibits growth and promotes apoptosis of HCC cells; BITC has a significant inhibitory effect on the migration and invasion of HCC cells. BITC stimulated expression of caspase-3/8 and PARP-1 and suppressed expression of survivin, MMP2/9 and CXCR4. BITC also inhibited the enzymatic activities of MMP2 and MMP9.

Conclusions

BITC was able to induce apoptosis and suppress the invasive and migratory abilities of Bel 7402 and HLE cells. The mechanism by which BITC is involved in these processes may include up-regulating the expression of apoptosis-related proteins and down-regulating the expression of metastasis-related proteins. BITC may be a novel chemotherapy for HCC patients.

Clinical trial indentification

Legal entity responsible for the study

Mengsen Li

Funding

the National Natural Science Foundation of China

Disclosure

All authors have declared no conflicts of interest.