Effect of β-phenylethyl isothiocyanate from cruciferous vegetables on growth inhibition and apoptosis of cervical cancer cells through the induction of death receptors 4 and 5
Huong le D, Shim JH, Choi KH, Shin JA, Choi ES, Kim HS, Lee SJ, Kim SJ, Cho NP, Cho SD
Journal of agricultural and food chemistry · 36 citations
Review labels
Neutral facts our review recorded about how this study was done. They describe method, never whether we like the result.
How it was studied
- Design
- In vitro/mechanistic study (classified by our AI screen)
- Studied in
- Cells or lab samples
- Main outcome
- Mechanisms only
Who paid for it
- Funding
- Funding not disclosed
Publication
- Published
- 2011-06-27 · J Agric Food Chem · vol. 59 · issue 15 · pp. 8124–8131
- Publisher
- American Chemical Society
- Cited
- 46 citations · more than 86% of similar papers · 2.1× the field average
- References
- 47 works
- Access
- Paywalled
- Research areas
- Genomics, phytochemicals, and oxidative stress · Garlic and Onion Studies · Nitrogen and Sulfur Effects on Brassica
- Keywords
- Phenethyl isothiocyanate, MAPK/ERK pathway, Apoptosis, Cruciferous vegetables, p38 mitogen-activated protein kinases, Programmed cell death, Kinase, Cancer research, Carcinogenesis, Isothiocyanate, Chemistry, Cancer cell, Biology, Cancer, Cell biology, Biochemistry
- MeSH
- cell line, tumor, humans, brassicaceae, vegetables, isothiocyanates, plant extracts, anticarcinogenic agents, apoptosis, cell proliferation, uterine cervical neoplasms, female, receptors, tnf-related apoptosis-inducing ligand
10 authors
From KR
- Le Diem HuongJeonbuk National University
- Jung-Hyung ShimSoonchunhyang University
- Kyeong‐Hee ChoiJeonbuk National University
- Ji‐Ae ShinJeonbuk National University
- Eun‐Sun ChoiJeonbuk National University
- Hyung‐Seop KimJeonbuk National University
Abstract
Cruciferous vegetables have been shown to have the possibility to protect against multistep carcinogenesis. β-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 DR5) 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 NH(2)-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 DR5 through the inactivation of ERK and MEK.
Abstract via Europe PMC. Copyright remains with the authors or publisher.
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