Document Detail


Growth arrest, apoptosis, and telomere shortening of Barrett's-associated adenocarcinoma cells by a telomerase inhibitor.
MedLine Citation:
PMID:  15131795     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND & AIMS: Barrett's esophageal adenocarcinoma (BEAC) is a complication of gastroesophageal reflux disease, with no effective chemotherapy and poor prognosis. BEAC cells, like many other types of cancers, may reactivate telomerase to achieve unlimited proliferative potential, making telomerase a unique therapeutic target. The purpose of this study was to evaluate effects of telomerase inhibition on BEAC. METHODS: We examined the effect of a selective G-quadruplex intercalating telomerase inhibitor, 2,6-bis[3-(N-Piperidino)propionamido]anthracene-9,10-dione (PPA), on telomerase activity, telomere length, colony size distribution, and proliferative potential in 2 BEAC cell lines, BIC-1 and SEG-1. RESULTS: Telomerase activity was >10-fold and >600-fold elevated in the adenocarcinoma cells as compared with normal gastric/intestinal cells and normal diploid fibroblasts, respectively. Telomeres were short, being less than 4 kilobase pair in both tumor cell lines. Exposure to PPA effectively inhibited telomerase activity and shortened telomeres. PPA also arrested cell proliferation and reduced colony number and size after a lag period of about 10 cell generations, consistent with the attrition of telomeres. The growth arrest was not due to senescence but was due to apoptosis. Expression analysis of the cells following PPA treatment did not show significant change in the expression of genes involved in cell-cycle proliferation and apoptosis. Exposure to PPA had no effect on proliferative potential of normal intestinal cells. CONCLUSIONS: We conclude that telomerase inhibition by PPA induces cell growth arrest in BEAC cells and demonstrate the potential of telomerase inhibitors in chemoprevention and treatment of Barrett's-associated esophageal adenocarcinoma.
Authors:
Masood A Shammas; Hemanta Koley; David G Beer; Cheng Li; Raj K Goyal; Nikhil C Munshi
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Gastroenterology     Volume:  126     ISSN:  0016-5085     ISO Abbreviation:  Gastroenterology     Publication Date:  2004 May 
Date Detail:
Created Date:  2004-05-07     Completed Date:  2004-06-23     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0374630     Medline TA:  Gastroenterology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1337-46     Citation Subset:  AIM; IM    
Affiliation:
VA Boston Health Care System, Boston, MA, USA.
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MeSH Terms
Descriptor/Qualifier:
Adenocarcinoma / etiology,  pathology,  physiopathology*
Anthraquinones / pharmacology*
Apoptosis* / drug effects
Barrett Esophagus / complications*
Cell Division / drug effects
Cell Line, Tumor
Enzyme Inhibitors / pharmacology*
Esophageal Neoplasms / etiology,  pathology,  physiopathology*
Gene Expression / drug effects
Gene Expression Profiling
Humans
Piperidines / pharmacology*
Stem Cells / pathology
Telomerase / antagonists & inhibitors*,  metabolism
Telomere / drug effects,  genetics*
Grant Support
ID/Acronym/Agency:
DK 031092/DK/NIDDK NIH HHS; P01 78378//PHS HHS; P50 CA 10070/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/2,6-bis(3-(N-piperidino)propionamido)anthracene-9,10-dione; 0/Anthraquinones; 0/Enzyme Inhibitors; 0/Piperidines; EC 2.7.7.49/Telomerase

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


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