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Carcinogenesis Advance Access published online on May 12, 2006
Carcinogenesis, doi:10.1093/carcin/bgl068
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© The Author 2006. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org
Received February 27, 2006
Revised April 27, 2006
Accepted April 27, 2006

CANCER BIOLOGY

Escaping from the TGF{beta} anti-proliferative control

Joan Seoane 1 *

1 Institució Catalana de Recerca i Estudis Avançats (ICREA), Medical Oncology Program, Vall d'Hebron University Hospital Research Institute, Barcelona

* To whom correspondence should be addressed.
Joan Seoane, E-mail: jseoane{at}ir.vhebron.net


  Abstract

Transforming growth factor-{beta} (TGF{beta}) has a crucial role in tissue homeostasis and disruption of the TGF{beta} pathway has been implicated in many human diseases including cancer. As a potent inhibitor of epithelial cell proliferation, TGF{beta} is a tumor suppressor. Tumor cells evade the anti-tumoral effect of TGF{beta}, either by acquiring somatic mutations that blunt TGF{beta} signaling or by selectively preventing the cytostatic responses to TGF{beta}. During tumor progression, TGF{beta} not only loses the anti-proliferative response but can become an oncogenic factor. Recent work has provided insights into the specific molecular mechanisms involved in the loss of the TGF{beta} anti-proliferative response. This review is an overview of the mechanisms that lead to the impairment of the tumor-suppressive function of TGF{beta} in cancer. The understanding of how the TGF{beta} signal is disrupted in cancer might facilitate the design and development of rational and successful therapeutic strategies.


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