NDLI: Activation of the apoptosis signal-regulating kinase 1/c-Jun N-terminal kinase pathway is involved in the casticin-induced apoptosis of colon cancer cells

Content Provider	PubMed Central
Author	Lin, Qu Liu, Feng-xia Cao, Xiao-cheng Xiao, Qiao Yang, Xiaohong Ren, Kai-qun
Copyright Year	2014
Abstract	Casticin is one of the main components of the fruits of Vitex rotundifolia L. Studies have shown that casticin inhibits the growth of various cancer cells, including colon cancer. In the present study, the anti-carcinogenic effects of casticin on human colon cancer and the underlying mechanisms were investigated. The results revealed that casticin significantly induced apoptosis of HT-29, HCT-116, SW480 and Caco-2 cells, induced the accumulation of reactive oxygen species (ROS) and increased the protein levels of apoptosis signal-regulating kinase 1 (ASK1), c-Jun N-terminal kinase (JNK) and B-cell lymphoma 2-interacting mediator of cell death (Bim) in HT-29 cells. Pretreatment with N-acetylcysteine, an antioxidant chemical compound, inhibited the activation of ASK1, JNK and Bim, as well as the apoptosis induced by casticin. Small interfering RNA targeting ASK1 significantly attenuated the induction of JNK and Bim activation and apoptotic cell death by casticin treatment. SP600125, a specific JNK inhibitor, attenuated Bim activation and apoptosis, but did not alter ASK1 phosphorylation levels. In addition, casticin treatment resulted in apoptosis by the same mechanism in HCT-116, SW480 and Caco-2 cells. These results suggest that casticin significantly induced apoptosis by the activation of the ASK1-JNK-Bim signaling cascade and the accumulation of ROS in colon cancer cells.
Related Links	http://dx.doi.org/10.3892/etm.2014.1934
Ending Page	1500
Page Count	7
Starting Page	1494
File Format	PDF
ISSN	17920981
e-ISSN	17921015
Journal	Experimental and Therapeutic Medicine
Issue Number	5
Volume Number	8
Language	English
Publisher	D.A. Spandidos
Publisher Date	2014-08-01
Access Restriction	Open
Rights Holder	D.A. Spandidos
Subject Keyword	Immunology and Microbiology (miscellaneous) Cancer Research Medicine(all) Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cancer Research 2400/2401

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