Authors:
A Bruna, RS Darken, F Rojo, A Ocaña, S Peñuelas, A Arias, R Paris, A Tortosa, J Mora, J Baselga, J Seoane
Journal name: 
Cancer Cell
Citation info: 
11(2):147-160
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.
DOI: 
http://doi.org/10.1016/j.ccr.2006.11.023
E-pub date: 
01 Feb 2007
Users with this publication listed: 
Alejandra Bruna