Article

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

Department of Pediatrics, University of Illinois at Chicago, Chicago, IL 60612, USA.
FEBS letters (impact factor: 3.54). 05/2012; 586(10):1510-5. DOI:10.1016/j.febslet.2012.04.009
Source: PubMed

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.

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Keywords

cell proliferation
 
colonization
 
constitutive active HIF
 
HIF-independent function
 
integrin
 
integrin/FAK signaling pathway
 
kidney
 
Knockdown
 
lung cancer cell proliferation
 
lung cancer cells
 
lung cancer development
 
overexpression
 
pVHL
 
pVHL promotes epithelial-mesenchymal transition
 
pVHL regulates lung cancer development
 
stable A549 cells
 
tail-vein injection model
 
tumor colonization
 
tumor suppressor
 
von Hippel-Lindau protein