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. 2007 Feb;11(2):147-60.
doi: 10.1016/j.ccr.2006.11.023.

High TGFbeta-Smad activity confers poor prognosis in glioma patients and promotes cell proliferation depending on the methylation of the PDGF-B gene

Alejandra Bruna  1 , Rachel S Darken, Federico Rojo, Alberto Ocaña, Silvia Peñuelas, Alexandra Arias, Raquel Paris, Avelina Tortosa, Jaume Mora, Jose Baselga, Joan Seoane
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Free article

High TGFbeta-Smad activity confers poor prognosis in glioma patients and promotes cell proliferation depending on the methylation of the PDGF-B gene

Alejandra Bruna et al. Cancer Cell. 2007 Feb.
Free article

Abstract

TGFbeta acts as a tumor suppressor in normal epithelial cells and early-stage tumors and becomes an oncogenic factor in advanced tumors. The molecular mechanisms involved in the malignant function of TGFbeta are not fully elucidated. We demonstrate that high TGFbeta-Smad activity is present in aggressive, highly proliferative gliomas and confers poor prognosis in patients with glioma. We discern the mechanisms and molecular determinants of the TGFbeta oncogenic response with a transcriptomic approach and by analyzing primary cultured patient-derived gliomas and human glioma biopsies. The TGFbeta-Smad pathway promotes proliferation through the induction of PDGF-B in gliomas with an unmethylated PDGF-B gene. The epigenetic regulation of the PDGF-B gene dictates whether TGFbeta acts as an oncogenic factor inducing PDGF-B and proliferation in human glioma.

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