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[Proc Amer Assoc Cancer Res, Volume 46, 2005]


Cellular and Molecular Biology 71: Signaling in Gastrointestinal Cancers

Abstract #5546

Interaction between the IGF and beta-catenin signaling pathways in esophageal carcinoma progression

Breda Kiely, Sharon McKenna and Gerald C. O’Sullivan

Cork Cancer Research Centre, BioSciences Institute, Cork, Ireland

Esophageal adenocarcinomas are highly malignant tumors with poor survival rates. However, the mechanisms which facilitate survival and metastasis of disseminated esophageal tumor cells are currently unknown. Abnormal expression of the E-cadherin/beta-catenin complex is common in esophageal adenocarcinoma. Insulin-like growth factors (IGFs) have been shown to modulate beta-catenin localization/activity in several cancer models. We have investigated the possible interplay between the IGFs and beta-catenin in esophageal carcinomas. We have demonstrated E-cadherin and beta-catenin expression in cell lines of both esophageal adenocarcinomas and squamous carcinomas. Adenocarcinomas were found to have lower levels of beta-catenin than squamous carcinomas. IGF-1 receptor (IGF-1R) expression was 1.2 to 2 fold greater on squamous carcinoma cells in comparison to adenocarcinoma cells, as determined by flow cytometric analysis. Expression of IGF ligands was determined by RT-PCR. IGF-2 mRNA was expressed in all esophageal carcinoma cells. However, IGF-1 mRNA was only detected in the squamous carcinoma cells. Serum deprivation reduced cell growth of these esophageal carcinoma cells and survival was maintained for several days in low serum conditions. Re-addition of increasing concentrations of IGF-1 or IGF-2 induced proliferation of these carcinoma cells as measured by 3H-thymidine incorporation, and activation of signaling molecules downstream of IGF. We subsequently investigated whether activation of this pathway influenced beta-catenin distribution in the various cell types. We currently have found no evidence of beta-catenin redistribution, and beta-catenin transcriptional activity (measured using the Topflash reporter assay system) has not been influenced by addition of IGF-ligands for up to 24 hours. Our data suggest that ligands for IGF-1R play an important role in the growth of esophageal cells, however our current data suggests that this signaling does not influence beta-catenin distribution or activity in these esophageal cell line models.







HOME HELP FEEDBACK HOW TO CITE ABSTRACTS ARCHIVE CME INFORMATION SEARCH
Cancer ResearchClinical Cancer Research
Cancer Epidemiology Biomarkers & PreventionMolecular Cancer Therapeutics
Molecular Cancer ResearchCancer Prevention Research
Cancer Prevention Journals PortalCancer Reviews Online
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Copyright © 2005 by the American Association for Cancer Research.