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- Title
Allyl Isothiocyanate Induces Cell Toxicity by Multiple Pathways in Human Breast Cancer Cells.
- Authors
Bo, Peng; Lien, Jin-Cherng; Chen, Ya-Yin; Yu, Fu-Shun; Lu, Hsu-Feng; Yu, Chun-Shu; Chou, Yu-Cheng; Yu, Chien-Chih; Chung, Jing-Gung
- Abstract
Isothiocyanates (ITCs) occur in many cruciferous vegetables. These compounds, which have significant anticancer actions, can induce apoptosis in different human cancer cell lines. In the present study, we investigated if allyl isothiocyanate (AITC) would induce toxicity in human breast cancer MCF-7 (estrogen receptor positive) and MDA-MB-231 (estrogen receptor negative) cells. We found that AITC stimulated reactive oxygen species and Ca production, and decreased the mitochondrial membrane potential. Activity of caspase-8, -9 and -3 was increased by AITC in both cell lines. AITC also induced mitochondrial-mediated apoptosis, as shown by cytochrome c, AIF and Endo G release from mitochondria, activation of caspase-9 and caspase-3, and formation of DAPI-positive cells. There was a significant reduction in the levels of the anti-apoptotic protein Bcl-2 along with a marked increase in the pro-apoptotic protein Bax in both cell lines. AITC induced apoptosis in human breast cancer MCF-7 cells via AIF and Endo G signaling pathways, but in MDA-MB-231 cells apoptosis occurred via the GADD153 pathway. This study has revealed novel anti-cancer mechanisms of AITC, a compound that is ordinarily present in human diets and may have potential therapeutic effects in various cancers.
- Subjects
TAIWAN; REACTIVE oxygen species; APOPTOSIS; BIOLOGICAL assay; BIOLOGICAL transport; BREAST tumors; CALCIUM; CELL culture; CELL cycle; CELL lines; CELL physiology; DNA; FLOW cytometry; MITOCHONDRIA; PROBABILITY theory; PROTEOLYTIC enzymes; RESEARCH funding; T-test (Statistics); WESTERN immunoblotting; PHYTOCHEMICALS; DATA analysis software; CYTOTOXINS; DESCRIPTIVE statistics
- Publication
American Journal of Chinese Medicine, 2016, Vol 44, Issue 2, p415
- ISSN
0192-415X
- Publication type
Article
- DOI
10.1142/S0192415X16500245