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 | Cancer Biology 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
|
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.