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Lysophosphatidylethanolamine acts on type 1 lysophosphatidic acid receptor in MDA‐MB‐231 breast cancer cells
Author(s) -
IM DONGSOON,
PARK SOOJIN,
LEE KYOUNGPIL
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.656.10
Subject(s) - lysophosphatidylethanolamine , lysophosphatidic acid , g protein coupled receptor , transfection , cancer cell , pertussis toxin , phospholipase d , lysophosphatidylcholine , microbiology and biotechnology , receptor , chemistry , phospholipase c , lipid signaling , cell culture , biology , g protein , biochemistry , phospholipid , signal transduction , cancer , phosphatidylcholine , genetics , membrane
Lysophosphatidylethanolamine (LPE) is a lyso‐type metabolite of phosphatidylethanolamine, a plasma membrane component. Actions of LPE have been implicated to be mediated through G‐protein‐ coupled receptor (GPCR). GPCRs for lysophosphatidic acid, a structurally‐similar representative lipid mediator, have not been implicated in LPE‐mediated actions in SK‐OV3 and OVCAR‐3 ovarian cancer cells and in the receptor over‐expression systems. In the present study, LPE‐induced intracellular Ca 2+ increase was observed in MDA‐MB‐231 cells but not other breast cancer cell lines. LPE‐ and LPA‐induced responses showed homologous and heterologous desensitization. Furthermore, antagonists for LPA 1 and LPA 3 , VPC32183 and Ki16425, inhibited LPE‐induced Ca 2+ increase and Knockdown of LPA 1 by transfection of LPA 1 siRNA also completely inhibited LPE‐induced Ca 2+ rise in the cells. Pertussis toxin, a specific inhibitor of G i/o proteins, edelfosin, an inhibitor of phospholipase C, 2‐APB, an inhibitor of IP 3 receptor, completely inhibited LPE‐induced response. However, HA130, an inhibitor of autotoxin/lysophospholipase D, did not inhibit the response. Therefore, LPE is supposed to act on LPA 1 /G i/o proteins/phospholipase C/IP 3 /Ca 2+ rise in MDA‐MB‐231 breast cancer cells. This work was supported by MRC program (2009–0083538) and by Basic Science Research Program (2011–0021158) of the NRF of Korea.