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Acta Biochimica et Biophysica Sinica Advance Access originally published online on September 3, 2009
Acta Biochimica et Biophysica Sinica 2009 41(10):839-845; doi:10.1093/abbs/gmp070
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© The Author 2009. Published by ABBS Editorial Office in association with Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.

Cortactin is involved in transforming growth factor-β1-induced epithelial-mesenchymal transition in AML-12 cells

Kehua Zhang, Dongmei Wang and Jianguo Song*

Laboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China

* Correspondence address. Tel: +86-21-54921167; Fax: +86-21-54921011; E-mail: jgsong{at}sibs.ac.cn


  Abstract

Cortactin is an F-actin binding protein, regulating cell movement and adhesive junction assembly. However, the function of cortactin in epithelial-mesenchymal transition (EMT) remains elusive. Here we found that during transforming growth factor-β1 (TGF-β1)-induced EMT in AML-12 murine hepatocytes, cortactin underwent tyrosine dephosphorylation. Inhibition of the dephosphorylation of cortactin by sodium vanadate blocked TGF-β1-induced EMT. Knockdown of cortactin by RNAi led to decrease of intercellular junction proteins E-cadherin and Zonula occludens-1 and induced expression of mesenchymal protein fibronectin. Additionally, knockdown of cortactin further promoted TGF-β1-induced EMT in AML-12 cells, as determined by EMT markers and cell morphological changes. Moreover, migration assay showed that cortactin knockdown promoted the migration of AML-12 cells, and also enhanced TGF-β1-induced migration. Our study showed the involvement of cortactin in the TGF-β1-induced EMT.

Keywords    epithelial-mesenchymal transition; cortactin; transforming growth factor-β; migration

Received: April 3, 2009; Accepted: May 31, 2009
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