Annals of Surgical Oncology Cite Track
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Breen, E.
Right arrow Articles by Mercurio, A. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Breen, E.
Right arrow Articles by Mercurio, A. M.

Annals of Surgical Oncology, Vol 2, Issue 5 378-385, Copyright © 1995 by Society of Surgical Oncology


ARTICLES

Role of the E-cadherin/alpha-catenin complex in modulating cell-cell and cell-matrix adhesive properties of invasive colon carcinoma cells

E. Breen, G. Steele Jr and A. M. Mercurio
Laboratory of Cancer Biology, New England Deaconess Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.

BACKGROUND: The clinical behavior of colorectal cancer depends on its ability to invade and metastasize. Metastatic cells must dissociate from other cells and invade through basement membrane and stroma. Cell-cell adhesion in epithelial cells is mediated by the cell surface protein E-cadherin in association with alpha- and beta-catenin, which link E-cadherin to the cytoskeleton. Decreased cell-cell adhesion and increased motility on laminin have been correlated with more poorly differentiated and aggressive carcinomas. METHODS: In this study, the RKO cell line, previously shown by us to lack E-cadherin expression, was transfected with the complementary DNA for E-cadherin. The transfectants were selected for high levels of surface expression by sequential FACS and examined in functional assays. RESULTS: In comparison to control transfectants, the E-cadherin transfectants exhibited a more epithelial-like morphology, a 30% increase in Ca(2+)-dependent cell-cell aggregation, and a markedly reduced motility on the matrix proteins, collagen I and laminin. CONCLUSIONS: These data demonstrate that correction of a defect in the cadherin/catenin cell-cell adhesion complex, often found in poorly differentiated and highly invasive tumors, facilitates increased cell-cell adhesion and retards tumor cell migration on basement membrane and stromal proteins.


This article has been cited by other articles:


Home page
Cancer Res.Home page
S. Chakrabarty, H. Wang, L. Canaff, G. N. Hendy, H. Appelman, and J. Varani
Calcium Sensing Receptor in Human Colon Carcinoma: Interaction with Ca2+ and 1,25-Dihydroxyvitamin D3
Cancer Res., January 15, 2005; 65(2): 493 - 498.
[Abstract] [Full Text] [PDF]


Home page
The OncologistHome page
M. A. Khan and A. W. Partin
Management of High-Risk Populations with Locally Advanced Prostate Cancer
Oncologist, June 1, 2003; 8(3): 259 - 269.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
D. B. Stewart and W. J. Nelson
Identification of Four Distinct Pools of Catenins in Mammalian Cells and Transformation-dependent Changes in Catenin Distributions among These Pools
J. Biol. Chem., November 21, 1997; 272(47): 29652 - 29662.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1995 by the Society of Surgical Oncology.