Icilin induces G1 arrest through activating JNK and p38 kinase in a TRPM8-independent manner

Title
Icilin induces G1 arrest through activating JNK and p38 kinase in a TRPM8-independent manner
Author(s)
전주홍[전주홍]박현호김수화[김수화]김성영[김성영]박은정[박은정]김준[김준]서인석[서인석]김선정[김선정]
Keywords
PROSTATE-CANCER CELLS; ANDROGEN RECEPTOR; PROTEIN-KINASES; CYCLE; PATHWAYS; TRPM8; PROGRESSION; THERAPIES; SURVIVAL; TARGETS
Issue Date
201103
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Citation
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.406, no.1, pp.30 - 35
Abstract
Aberrant regulation of cell cycle confers a limitless replicative potential, which is a hallmark of cancer. Currently, the compounds targeting the cell cycle are undergoing cancer clinical trials. In this study, we demonstrated that icilin, a cooling compound, induces Cl arrest in PC-3 prostate cancer cells without cell death. Icilin modulated the expression level of various cell cycle regulators at transcription or post-translational levels. In addition, icilin activated JNK and p38 kinase pathways, but not ERK. Both JNK and p38 kinases cooperatively mediated icilin-induced Cl arrest, which was rescued by pharmacologic inhibition of these kinases. The action of icilin on Cl arrest was unrelated to the activation of TRPM8 calcium channel. Our findings suggest that icilin is a valuable chemical probe for future investigation aiming at delineating the molecular mechanisms of cell cycle regulation in prostate cancer. (C) 2011 Elsevier Inc. All rights reserved.
URI
http://hdl.handle.net/YU.REPOSITORY/25577http://dx.doi.org/10.1016/j.bbrc.2011.01.094
ISSN
0006-291X
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이과대학 > 화학생화학부 > Articles
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