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Knockdown of von Hippel-Lindau Protein decreases lung cancer cell proliferation and colonization

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Title: Knockdown of von Hippel-Lindau Protein decreases lung cancer cell proliferation and colonization
Author(s): Zhou, Qiyuan; Chen, Tianji; Ibe, Joyce Christina F.; Raj, J Usha; Zhou, Guofei
Subject(s): focal adhesion protein integrin von Hippel-Lindau protein
Abstract: Although von Hippel-Lindau protein (pVHL) is known as a tumor suppressor in kidney and other organs, it remains unclear whether pVHL plays a role in lung cancer development. We investigated the role of pVHL in lung cancer cell proliferation, migration, and colonization using stable A549 cells with knockdown of pVHL. We found that knockdown of pVHL promotes epithelial-mesenchymal transition (EMT) in lung cancer cells. Knockdown of pVHL decreased tumor colonization in a tail-vein injection model and decreased cell proliferation, whereas overexpression of constitutive active HIF increased tumor colonization, suggesting a HIF-independent function of pVHL in lung. Knockdown of pVHL decreased phosphorylation of FAK and expression of integrin, suggesting that pVHL regulates lung cancer development via integrin/FAK signaling pathway.
Issue Date: 2012-05
Publisher: Elsevier
Citation Info: Zhou Q, Chen T, Ibe JC, Raj JU, Zhou G. Knockdown of von Hippel-Lindau protein decreases lung cancer cell proliferation and colonization. FEBS Letters. 2012 May 21;586(10):1510-5. Epub 2012 Apr 20. DOI: 10.1016/j.febslet.2012.04.009
Type: Article
Description: NOTICE: this is the author’s version of a work that was accepted for publication in FEBS Letters. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in FEBS Letters, [Vol 586, Issue 10, 2012, May] DOI:10.1016/j.febslet.2012.04.009
ISSN: 1873-3468
Sponsor: The work was supported in part by the University of Illinois at Chicago Faculty Scholarship Support Program (GZ), the University of Illinois Cancer Center Pilot Subsidy Program, and supplemental funding from the UIC Center for Clinical and Translational Science (UL1RR029879). This project started at the laboratory of Dr. Jacob I. Sznajder at the Northwestern University.
Date Available in INDIGO: 2012-10-02

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