期刊
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS
卷 1736, 期 3, 页码 228-236出版社
ELSEVIER
DOI: 10.1016/j.bbalip.2005.08.009
关键词
5-Oxo-ETE; 5-HETE; cancer cell; proliferation; apoptosis; PPAR
资金
- NCI NIH HHS [CA77489, CA70338] Funding Source: Medline
- NIEHS NIH HHS [ES11124, TS ES07331] Funding Source: Medline
- FDA HHS [BM61754] Funding Source: Medline
MDA-MB-231, MCF7, and SKOV3 cancer cells, but not HEK-293 cells, expressed mRNA for the leukocyte G protein-coupled 5-oxo-eicosatetracnoate (ETE) OXE receptor. 5-Oxo-ETE, 5-oxo-15-OH-ETE, and 5-HETE stimulated the cancer cell lines but not HEK-293 cells to mount pertussis toxin-sensitive proliferation responses. Their potencies in eliciting this response were similar to their known potencies in activating leukocytes and OXE receptor-transfected cells. However, high concentrations of 5-oxo-ETE and 5-oxo-15-OHETE, but not 5-HETE, arrested growth and caused apoptosis in all four cell lines; these responses were pertussis toxin-resistant. The same high concentrations of the oxo-ETEs but again not 5-HETE also activated peroxisome proliferator-activated receptor (PPAR)-gamma. Pharmacological studies indicated that this activation did not mediate their effects on proliferation. These results are the first to implicate the OXE receptor in malignant cell growth and to show that 5-oxo-ETEs activate cell death programs as well as PPAR-gamma independently of this receptor. (c) 2005 Elsevier B.V. All rights reserved.
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