期刊
CANCER BIOLOGY & THERAPY
卷 3, 期 2, 页码 221-225出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/cbt.3.2.666
关键词
p21; TGF-beta; arrest; proliferation; breast cancer
类别
资金
- NCI NIH HHS [P50 CA88843, P50 CA58236] Funding Source: Medline
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.
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