丝切蛋白-1的过表达以R-钙黏蛋白依赖的方式恢复MDA-MB-231乳腺癌细胞中的黏着连接。
Profilin-1 overexpression restores adherens junctions in MDA-MB-231 breast cancer cells in R-cadherin-dependent manner.
作者信息
Zou Li, Hazan Rachel, Roy Partha
机构信息
Department of Bioengineering, University of Pittsburgh, 306 Center for Bioengineering, 300 Technology Drive, Pittsburgh, PA 15219, USA.
出版信息
Cell Motil Cytoskeleton. 2009 Dec;66(12):1048-56. doi: 10.1002/cm.20407.
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.
摘要
丝切蛋白-1（Pfn1）是一种广泛表达的肌动蛋白结合蛋白，在几种不同类型的腺癌中表达下调，并对乳腺癌细胞系产生肿瘤抑制作用。MDA-MB-231（MDA-231）是一种乳腺癌细胞系，具有上皮-间质转化后的所有特征，不形成细胞间粘附，通过Pfn1过表达可恢复为上皮样表型。这种形态转变是由粘着连接（AJ）的恢复引起的，这需要Pfn1与肌动蛋白相互作用。Pfn1过表达增加了R-钙粘蛋白（一种在亲代细胞系中内源性表达的钙粘蛋白）的表达水平，并以R-钙粘蛋白依赖的方式恢复MDA-231细胞中的AJ。这些发现突出了Pfn1在调节上皮细胞间粘附方面的重要作用。
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