Loss of Coxsackie and adenovirus receptor downregulates α-catenin expression

16Citations
Citations of this article
29Readers
Mendeley users who have this article in their library.

Abstract

Background: The Coxsackie and adenovirus receptor (CAR) has been shown to inhibit cancer cell proliferation, migration, and invasion. The underlying mechanisms, however, are poorly understood.Methods:The differential gene expression in the human colon cancer cell line DLD1 on RNAi-mediated functional CAR knockdown was analysed using oligo-array technology. Expression of α-catenin was determined by quantitative RT-PCR and western blotting. Proliferation, migration, and invasion after CAR knockdown were assessed by in vitro assays, and cell morphology in a three-dimensional context was evaluated using matrigel.Results:Oligo-array technology identified α-catenin as the strongest downregulated gene after CAR knockdown. Western blotting and quantitative RT-PCR confirmed a reduced α-catenin expression after CAR knockdown in DLD1 cells and in the rat intestinal cell line IEC-6. Functionally, both cell lines showed a marked increase in proliferation, migration, and invasion on CAR knockdown. In matrigel, both cell lines formed amorphous cell clusters in contrast to well-organised three-dimensional structures of CAR-expressing vector controls. Ectopic re-expression of α-catenin in DLD1 and IEC-6 CAR knockdown cells reversed these functional and morphological effects.ConclusionThese data suggest that an interaction of CAR and α-catenin mediates the impact of CAR on cell proliferation, migration, invasion, and morphology. © 2009 Cancer Research UK All rights reserved.

Cite

CITATION STYLE

APA

Stecker, K., Koschel, A., Wiedenmann, B., & Anders, M. (2009). Loss of Coxsackie and adenovirus receptor downregulates α-catenin expression. British Journal of Cancer, 101(9), 1574–1579. https://doi.org/10.1038/sj.bjc.6605331

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free