Document Detail

ERBB2 suppression decreases cell growth via apoptosis in gastrointestinal adenocarcinomas.
MedLine Citation:
PMID:  19628076     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Although the incidence of adenocarcinoma of the esophageal and gastroesophageal junction has increased at an alarming rate in the past 30 years, little improvement has been made in treatment strategies. Previous studies have demonstrated that many upper gastrointestinal (GI) adenocarcinomas exhibit ERBB2 amplification. In cancers proven to have similar amplification, such as breast, ERBB2-targeted therapies have dramatically improved overall survival and disease-free rates of survival. This study uses siRNA to knockdown ERBB2 in GI adenocarcinoma cell lines to evaluate cell viability, apoptosis, and changes in cell cycle. METHODS: A cell line with a baseline amount of ERBB2 (Seg-1) and 2 upper GI adenocarcinoma cell lines with known amplification of ERBB2 (esophageal [OE19] and gastric [MKN45]) were treated with 120 pmol of 1 of 2 independent ERBB2 siRNAs or control siRNA for 6 hours. RESULTS: We demonstrate that knockdown of ERBB2 in esophageal and gastric cancer cell lines with known ERBB2 amplification effectively decreases ERBB2 protein levels and decreases cell viability mainly via apoptotic pathways. CONCLUSION: ERBB-directed therapy may be of benefit in the subset of patients with GI adenocarcinomas exhibiting amplification of ERBB2.
Amanda K Arrington; Peter S Dahlberg; Julia Davydova; Selwyn M Vickers; Masato Yamamoto
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Surgery     Volume:  146     ISSN:  1532-7361     ISO Abbreviation:  Surgery     Publication Date:  2009 Aug 
Date Detail:
Created Date:  2009-07-24     Completed Date:  2009-08-18     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0417347     Medline TA:  Surgery     Country:  United States    
Other Details:
Languages:  eng     Pagination:  213-9     Citation Subset:  AIM; IM    
Department of Surgery, University of Minnesota, Minneapolis, MN 55455, USA.
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MeSH Terms
Adenocarcinoma / genetics*,  metabolism,  pathology
Cell Cycle
Cell Line, Tumor
Cell Survival
Esophageal Neoplasms / genetics*,  metabolism,  pathology
Esophagogastric Junction*
Gene Amplification
Gene Expression
Gene Knockdown Techniques
RNA, Messenger / metabolism
RNA, Small Interfering
Receptor, erbB-2 / genetics*,  metabolism
Reverse Transcriptase Polymerase Chain Reaction
Stomach Neoplasms / genetics*,  metabolism,  pathology
Tumor Cells, Cultured
Grant Support
Reg. No./Substance:
0/RNA, Messenger; 0/RNA, Small Interfering; EC, erbB-2

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

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