期刊
CANCER LETTERS
卷 336, 期 1, 页码 185-195出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2013.04.027
关键词
5-Lipoxygenase; Apoptosis; 5-OxoETE; OXER1; PLC-beta; PKC-epsilon
类别
资金
- National Cancer Institute of the National Institutes of Health [RO1 CA152334]
- United States Department of Defense Prostate Cancer Research Program [DAMD 17-02-1-0153, W81-XWH-05-1-0022]
- Henry Ford Health System internal research Grant [A10203]
Inhibition of 5-Lox induces apoptosis in prostate cancer cells by inactivating PKC epsilon which is prevented by 5-oxoETE, and activators of PKC epsilon prevent 5-Lox inhibition-induced apoptosis, suggesting that 5-Lox metabolites exert survival signaling via PKC epsilon. However, mechanisms by which 5-Lox metabolites activate PKC epsilon are not understood yet. We found that prostate cancer cells express high levels of OXER1, a G protein-coupled 5-oxoETE receptor, which delivers signal by generating diacyl-glycerol through phospholipase C-beta. Interestingly, we found that U73122, an inhibitor of PLC-beta, interrupts the apoptosis-preventing effect of 5-oxoETE, and exogenous diacyl-glycerol effectively prevents 5-Lox inhibition-induced apoptosis, suggesting that 5-oxoETE signals via OXER1 to promote prostate cancer cell survival. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
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