© 2000 by Oxford University Press
Journal of the National Cancer Institute, Vol. 92, No. 17, 1388-1402,
September 6, 2000
© 2000 Oxford University Press
REVIEW |
Role of Transforming Growth Factor-ß Signaling in Cancer
Affiliation of authors: Laboratory of Cell Regulation and Carcinogenesis, Division of Basic Sciences, National Cancer Institute, Bethesda, MD.
Correspondence to: Anita B. Roberts, Ph.D., National Institutes of Health, Bldg. 41, Rm. C629, 41 Library Drive, MSC 5055, Bethesda, MD 20892-5055 (e-mail: (Robertsa{at}dce41.nci.nih.gov).
Signaling from transforming growth factor-ß (TGF-ß) through its unique transmembrane receptor serine–threonine kinases plays a complex role in carcinogenesis, having both tumor suppressor and oncogenic activities. Tumor cells often escape from the antiproliferative effects of TGF-ß by mutational inactivation or dysregulated expression of components in its signaling pathway. Decreased receptor function and altered ratios of the TGF-ß type I and type II receptors found in many tumor cells compromise the tumor suppressor activities of TGF-ß and enable its oncogenic functions. Recent identification of a family of intracellular mediators, the Smads, has provided new paradigms for understanding mechanisms of subversion of TGF-ß signaling by tumor cells. In addition, several proteins recently have been identified that can modulate the Smad-signaling pathway and may also be targets for mutation in cancer. Other pathways such as various mitogen-activated protein kinase cascades also contribute substantially to TGF-ß signaling. Understanding the interplay between these signaling cascades as well as the complex patterns of cross-talk with other signaling pathways is an important area of investigation that will ultimately contribute to understanding of the bifunctional tumor suppressor/oncogene role of TGF-ß in carcinogenesis.
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 G. Guillerm, E. Gyan, D. Wolowiec, T. Facon, H. Avet-Loiseau, K. Kuliczkowski, F. Bauters, P. Fenaux, and B. Quesnel p16INK4a and p15INK4b gene methylations in plasma cells from monoclonal gammopathy of undetermined significance Blood, July 1, 2001; 98(1): 244 - 246. [Abstract] [Full Text] [PDF]
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 C. Li, J. M. Garland, and S. Kumar Re: Role of Transforming Growth Factor-{{beta}} Signaling in Cancer J Natl Cancer Inst, April 4, 2001; 93(7): 555 - 556. [Full Text] [PDF]
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D. K. Lee, S. H. Park, Y. Yi, S.-G. Choi, C. Lee, W. T. Parks, H. Cho, M. P. de Caestecker, Y. Shaul, A. B. Roberts, et al. The hepatitis B virus encoded oncoprotein pX amplifies TGF-{beta} family signaling through direct interaction with Smad4: potential mechanism of hepatitis B virus-induced liver fibrosis Genes & Dev., February 15, 2001; 15(4): 455 - 466. [Abstract] [Full Text]
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 S. Itoh, J. Ericsson, J.-i. Nishikawa, C.-H. Heldin, and P. t. Dijke The transcriptional co-activator P/CAF potentiates TGF-{beta}/Smad signaling Nucleic Acids Res., November 1, 2000; 28(21): 4291 - 4298. [Abstract] [Full Text] [PDF]
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D. Saha, P. K. Datta, and R. D. Beauchamp Oncogenic Ras Represses Transforming Growth Factor-beta /Smad Signaling by Degrading Tumor Suppressor Smad4 J. Biol. Chem., July 27, 2001; 276(31): 29531 - 29537. [Abstract] [Full Text] [PDF]
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E. Piek, W. J. Ju, J. Heyer, D. Escalante-Alcalde, C. L. Stewart, M. Weinstein, C. Deng, R. Kucherlapati, E. P. Bottinger, and A. B. Roberts Functional Characterization of Transforming Growth Factor beta Signaling in Smad2- and Smad3-deficient Fibroblasts J. Biol. Chem., June 1, 2001; 276(23): 19945 - 19953. [Abstract] [Full Text] [PDF]
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K. L. Woodford-Richens, A. J. Rowan, P. Gorman, S. Halford, D. C. Bicknell, H. S. Wasan, R. R. Roylance, W. F. Bodmer, and I. P. M. Tomlinson SMAD4 mutations in colorectal cancer probably occur before chromosomal instability, but after divergence of the microsatellite instability pathway PNAS, August 14, 2001; 98(17): 9719 - 9723. [Abstract] [Full Text] [PDF]
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