Journal
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
Volume 59, Issue 15, Pages 8124-8131Publisher
AMER CHEMICAL SOC
DOI: 10.1021/jf2006358
Keywords
PEITC; cervical cancer cells; death receptors; ERK1/2; MEK
Funding
- Ministry of Education, Science and Technology [M10870050003-08N7005-00311, 2010-0007598]
- National Research Foundation of Korea [2010-0007598] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Cruciferous vegetables have been shown to have the possibility to protect against multistep carcinogenesis. beta-Phenylethyl isothiocyanate (PEITC) is one component of these vegetables demonstrated to help fight many types of cancer. The present study examined the apoptotic effects of PEITC and its molecular mechanism in human cervical cancer cell lines (HEp-2 and KB). PEITC induced apoptosis to inhibit cell proliferation. According to the protein chip assay, PEITC increased the expression of the death receptors (DR4 and DRS) and cleaved caspase-3 compared to the DMSO treatment group. PEITC also induced caspase-8 and truncated BID. PEITC down-regulated the phosphorylation of extracellular-related kinase (ERK)1/2, whereas neither phospho-c-Jun NH2-terminal kinases (JNK) nor phospho-p38 MAPK was changed. The role of ERK in PEITC-induced apoptosis was also investigated using MEK inhibitor (PD98059). PD98059 increased the expression of DR4 and DR5, activated caspase-3, and cleaved PARP. In addition, PEITC decreased the phosphorylation of MEK. Therefore, the apoptotic mechanism of PEITC in cervical cancer cells involves the induction of DR4 and DRS through the inactivation of ERK and MEK.
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