Document Detail

Modulation of growth in human esophageal adenocarcinoma cells by group IIa secretory phospholipase A(2).
MedLine Citation:
PMID:  20176206     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: Esophageal adenocarcinoma is thought to arise from lesions produced by chronic esophageal inflammation. Secretory phospholipase A(2) is an important mediator of mucosal response to gastroesophageal reflux, but its role in the function of mature cancer cells is unclear. We sought to determine the influence of group IIa secretory phospholipase A(2) on proliferation of human esophageal adenocarcinoma cells. METHODS: FLO-1 and OE33 cells derived from human esophageal adenocarcinoma were cultured with standard techniques. Cells were treated with 1-, 5-, 10-, and 20-mumol/L doses of 5-(4-benzyloxyphenyl)-4S-(7-phenylheptanoylamino)pentanoic acid, a specific inhibitor of group IIa secretory phospholipase A(2), for 72 hours. Gene for group IIa secretory phospholipase A(2)(PLA2G2A) was overexpressed and silenced with lentiviral infection techniques. Cell proliferation and viability were measured with standard 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide and bromodeoxyuridine incorporation assays. All assays were performed in triplicate. PLA2G2A expression was measured with quantitative reverse transcriptase polymerase chain reaction; protein levels were detected with immunofluorescence microscopy. Statistical analysis was by analysis of variance with Fisher post hoc analysis. RESULTS: Secretory phospholipase A(2) protein was found in both malignant esophageal adenocarcinoma cell lines. Treatment with specific group IIa secretory phospholipase A(2) inhibitor resulted in dose-dependent reductions in growth and cell number in both cell lines. Overexpression of PLA2G2A resulted in enhanced cancer cell growth, whereas gene knockdown attenuated growth. CONCLUSIONS: Group IIa secretory phospholipase A(2) appears significant in growth and proliferation of human esophageal adenocarcinoma cells. Secretory phospholipase A(2) inhibition should be studied further regarding potential chemopreventive and therapeutic properties in esophageal adenocarcinoma.
David Mauchley; Xianzhong Meng; Thomas Johnson; David A Fullerton; Michael J Weyant
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of thoracic and cardiovascular surgery     Volume:  139     ISSN:  1097-685X     ISO Abbreviation:  J. Thorac. Cardiovasc. Surg.     Publication Date:  2010 Mar 
Date Detail:
Created Date:  2010-02-23     Completed Date:  2010-04-01     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0376343     Medline TA:  J Thorac Cardiovasc Surg     Country:  United States    
Other Details:
Languages:  eng     Pagination:  591-9; discussion 599     Citation Subset:  AIM; IM    
Copyright Information:
Copyright 2010 The American Association for Thoracic Surgery. Published by Mosby, Inc. All rights reserved.
Department of Surgery, Division of Cardiothoracic Surgery, University of Colorado Denver School of Medicine, Aurora, CO, USA.
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MeSH Terms
Adenocarcinoma / enzymology*,  pathology*
Cell Proliferation
Esophageal Neoplasms / enzymology*,  pathology*
Group II Phospholipases A2 / physiology*
Tumor Cells, Cultured
Reg. No./Substance:
EC II Phospholipases A2

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

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