Document Detail


Overexpression of edg-2/vzg-1 induces apoptosis and anoikis in ovarian cancer cells in a lysophosphatidic acid-independent manner.
MedLine Citation:
PMID:  10632375     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Lysophosphatidic acid (LPA) is one of the major growth factors in ascites from ovarian cancer patients and appears to play an important role in proliferation, survival, and invasion of ovarian cancer cells. Recently, several groups have shown that Edg-2, which belongs to the G-protein coupled receptor family, is a functional LPA receptor. Northern blot analysis showed that most ovarian cancer cell lines express Edg-2. Edg-2 expression was especially high in the cisplatin-resistant and slowly proliferating 2780cp cell line and was almost absent from the cisplatin-sensitive and rapidly proliferating A2780 cell line. We thus assessed whether Edg-2 could contribute to changes in cell viability, cell proliferation, or cisplatin resistance. Stable overexpression of Edg-2 in A2780 cells induced an exogenous LPA-independent decrease in proliferation but did not alter cisplatin sensitivity. The LPA-independent decrease in growth rate induced by overexpression of Edg-2 could be explained, at least in part, by Edg-2-induced apoptosis rather than by effects on cell cycle progression. In agreement with the results in stably transfected A2780 cells, transient expression of Edg-2 in Jurkat T cells also induced apoptosis. When cells were separated from the extracellular matrix, they underwent a specialized form of apoptosis called anoikis, which is particularly important in survival of cells in the circulation during metastasis. A2780 cells engineered to overexpress Edg-2 were particularly sensitive to anoikis. These observations suggest that Edg-2 may be a negative regulator for ovarian epithelial cell growth and metastasis.
Authors:
T Furui; R LaPushin; M Mao; H Khan; S R Watt; M A Watt; Y Lu; X Fang; S Tsutsui; Z H Siddik; R C Bast; G B Mills
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Clinical cancer research : an official journal of the American Association for Cancer Research     Volume:  5     ISSN:  1078-0432     ISO Abbreviation:  Clin. Cancer Res.     Publication Date:  1999 Dec 
Date Detail:
Created Date:  2000-02-14     Completed Date:  2000-02-14     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  9502500     Medline TA:  Clin Cancer Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  4308-18     Citation Subset:  IM    
Affiliation:
Department of Molecular Oncology, University of Texas M.D. Anderson Cancer Center, Houston 77054, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antineoplastic Agents / pharmacology
Apoptosis*
COS Cells
Cell Division
Cisplatin / pharmacology
Drug Resistance, Neoplasm
Female
Humans
Jurkat Cells
Lysophospholipids / pharmacology,  physiology*
Mice
Nuclear Proteins / biosynthesis*,  genetics,  physiology
Ovarian Neoplasms / metabolism*,  pathology*
RNA, Messenger / genetics,  metabolism
Receptors, Cell Surface*
Receptors, G-Protein-Coupled*
Receptors, Lysophosphatidic Acid
Transcription Factors / biosynthesis*,  genetics,  physiology
Tumor Cells, Cultured
Grant Support
ID/Acronym/Agency:
CA64602/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Antineoplastic Agents; 0/Lysophospholipids; 0/Nuclear Proteins; 0/RNA, Messenger; 0/Receptors, Cell Surface; 0/Receptors, G-Protein-Coupled; 0/Receptors, Lysophosphatidic Acid; 0/Transcription Factors; 15663-27-1/Cisplatin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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