Volume 66, Issue 12 pp. 1048-1056
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Profilin-1 overexpression restores adherens junctions in MDA-MB-231 breast cancer cells in R-cadherin-dependent manner

Li Zou

Li Zou

Department of Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania

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Rachel Hazan

Rachel Hazan

Department of Pathology, Albert Einstein College of Medicine, Bronx, New York

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Partha Roy

Corresponding Author

Partha Roy

Department of Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania

Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania

Department of Bioengineering, University of Pittsburgh, 306 Center for Bioengineering, 300 Technology Drive, Pittsburgh, PA 15219, USASearch for more papers by this author
First published: 10 July 2009
Citations: 21

Abstract

Profilin-1 (Pfn1), a ubiquitously expressed actin-binding protein, is downregulated in several different types of adenocarcinoma and elicits tumor-suppressive effect on breast cancer cell lines. MDA-MB-231 (MDA-231), a breast cancer cell line that displays all the characteristics of post-epithelial-to-mesenchymal transition and does not form cell–cell adhesion, can be reverted to an epithelioid phenotype by Pfn1 overexpression. This morphological transition is caused by restoration of adherens junctions (AJ) requiring Pfn1's interaction with actin. Pfn1 overexpression increases the expression level of R-cadherin (a type of cadherin that is endogenously expressed in the parental cell line) and restores AJ in MDA-231 cells in R-cadherin-dependent manner. These findings highlight important role of Pfn1 in the regulation of epithelial cell–cell adhesion. Cell Motil. Cytoskeleton 2009. © 2009 Wiley-Liss, Inc.

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