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beta-Phenethyl isothiocyanate induces death receptor 5 to induce apoptosis in human oral cancer cells via p38

Authors
Huong, L. D.Shin, J-AChoi, E-SCho, N-PKim, H. M.Leem, D-HCho, S-D
Issue Date
Jul-2012
Publisher
WILEY
Keywords
human oral cancer cells; ss-phenylethyl isothiocyanate; apoptosis; death receptor 5; p38 MAPK
Citation
ORAL DISEASES, v.18, no.5, pp.513 - 519
Journal Title
ORAL DISEASES
Volume
18
Number
5
Start Page
513
End Page
519
URI
https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/16289
DOI
10.1111/j.1601-0825.2012.01905.x
ISSN
1354-523X
Abstract
Oral Diseases (2012) 18, 513519 Objectives: beta-Phenylethyl isothiocyanate (PEITC) has been demonstrated to fight many types of cancers through various molecular pathways. In this study, we focused on its effect on the induction of apoptosis to inhibit cell growth and molecular mechanism in oral cancer. Materials and methods: 3-(4,5-dimethylthiazol-2-yl)-5-(2,4-disulfophenyl)-2-(4 sulfophenyl)-2H-tetrazolium (MTS) assay was used to examine cell viability. The apoptotic effect was investigated using 4'-6-Diamidino-2-phenylindole (DAPI) staining or Western blotting. Inhibitors were used to determine the molecular target and mechanism of PEITC-mediated apoptosis. Results: beta-Phenylethyl isothiocyanate inhibited the growth of HN22 human oral cancer cells and induced caspase-dependent apoptosis in HN22 cells as evidenced by nuclear fragmentation and the activation of caspase 3. It increased cleaved caspase 8, truncated BID, and death receptor 5 (DR5) through the activation of p38 MAPK. This result was confirmed by blockage of PEITC-induced cleavages of Poly(ADP-ribose) Polymerase, caspase-3, caspase-8, and DR5 by p38 MAPK inhibitor, SB203580. We also found that PEITC activated p38 and augmented DR5 to induce apoptosis in other human oral cancer cells. Conclusions: These results suggest that DR5 is a potential molecular target for PEITC-induced apoptosis in oral cancer via p38 MAPK.
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