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Profilin‐1 overexpression restores adherens junctions in MDA‐MB‐231 breast cancer cells in R‐cadherin‐dependent manner
Author(s) -
Zou Li,
Hazan Rachel,
Roy Partha
Publication year - 2009
Publication title -
cell motility and the cytoskeleton
Language(s) - English
Resource type - Journals
eISSN - 1097-0169
pISSN - 0886-1544
DOI - 10.1002/cm.20407
Subject(s) - adherens junction , biology , cadherin , microbiology and biotechnology , profilin , actin cytoskeleton , cancer research , epithelial–mesenchymal transition , cell adhesion , actin , cell , cell culture , cytoskeleton , cancer , metastasis , genetics
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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