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Reversible Smad-Dependent Signaling between Tumor Suppression and Oncogenesis

1 Jun 2007

Abstract excerpt

Cancer cells often gain advantage by reducing the tumor-suppressive activity of transforming growth factor-beta (TGF-beta) together with stimulation of its oncogenic activity as in Ras-transformed cells; however, molecular mechanisms remain largely unknown. TGF-beta activates both its type I receptor (TbetaRI) and c-Jun NH2-terminal kinase (JNK), which phosphorylate Smad2 and Smad3 at the COOH-terminal...

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PMID: 17545585
DOI: 10.1158/0008-5472.can-06-4629

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