| Literature DB >> 14726675 |
Kurtis E Bachman1, Brian G Blair, Keith Brenner, Alberto Bardelli, Sabrina Arena, Shibin Zhou, Jessica Hicks, Angelo M De Marzo, Pedram Argani, Ben Ho Park.
Abstract
We investigated the mechanism by which cancers evade the growth inhibitory effects of TGF-beta. Using two p21-/- somatically deleted human epithelial cell lines, we find that TGF-beta serves as a growth stimulator rather than a growth suppressor to cells lacking p21. In addition, TGF-beta stimulated p21-/- cells exhibited a mesenchymal phenotype, demonstrated by an upregulation of vimentin and decreased expression of E-cadherin. Analysis of primary human breast cancers by immunohistochemical labeling confirmed a correlation between p21 loss and positive vimentin expression. These data provide a molecular mechanism explaining how nongastrointestinal cancers can escape the anti-proliferative effects of this cytokine and simultaneously use this pathway for growth advantage.Entities:
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Year: 2004 PMID: 14726675 DOI: 10.4161/cbt.3.2.666
Source DB: PubMed Journal: Cancer Biol Ther ISSN: 1538-4047 Impact factor: 4.742