Back to Search
Start Over
Phenethyl Isothiocyanate (PEITC) Inhibits the Growth of Human Oral Squamous Carcinoma HSC-3 Cells through G0/G1 Phase Arrest and Mitochondria-Mediated Apoptotic Cell Death
- Source :
- Evidence-Based Complementary and Alternative Medicine, Vol 2012 (2012)
- Publication Year :
- 2012
- Publisher :
- Hindawi Publishing Corporation, 2012.
-
Abstract
- Phenethyl isothiocyanate (PEITC), an effective anticancer and chemopreventive agent, has been reported to inhibit cancer cell growth through cell-cycle arrest and induction of apoptotic events in various human cancer cells models. However, whether PEITC inhibits human oral squamous cell carcinoma HSC-3 cell growth and its underlying mechanisms is still not well elucidated. In the present study, we evaluated the inhibitory effects of PEITC in HSC-3 cells and examined PEITC-modulated cell-cycle arrest and apoptosis. The contrast-phase and flow cytometric assays were used for examining cell morphological changes and viability, respectively. The changes of cell-cycle and apoptosis-associated protein levels were determined utilizing Western blotting in HSC-3 cells after exposure to PEITC. Our results indicated that PEITC effectively inhibited the HSC-3 cells’ growth and caused apoptosis. PEITC induced G0/G1 phase arrest through the effects of associated protein such as p53, p21, p17, CDK2 and cyclin E, and it triggered apoptosis through promotion of Bax and Bid expression and reduction of Bcl-2, leading to decrease the levels of mitochondrial membrane potential (ΔΨm), and followed the releases of cytochrome c, AIF and Endo G then for causing apoptosis in HSC-3 cells. These results suggest that PEITC could be an antitumor compound for oral cancer therapy.
- Subjects :
- Article Subject
lcsh:Other systems of medicine
lcsh:RZ201-999
Subjects
Details
- Language :
- English
- ISSN :
- 1741427X
- Database :
- OpenAIRE
- Journal :
- Evidence-Based Complementary and Alternative Medicine
- Accession number :
- edsair.dedup.wf.001..76293da54ea1062eac8b5bb609465abf
- Full Text :
- https://doi.org/10.1155/2012/718320