Inscrição na biblioteca: Guest
Portal Digital Begell Biblioteca digital da Begell eBooks Diários Referências e Anais Coleções de pesquisa
Critical Reviews™ in Eukaryotic Gene Expression
Fator do impacto: 2.156 FI de cinco anos: 2.255 SJR: 0.649 SNIP: 0.599 CiteScore™: 3

ISSN Imprimir: 1045-4403
ISSN On-line: 2162-6502

Volumes:
Volume 30, 2020 Volume 29, 2019 Volume 28, 2018 Volume 27, 2017 Volume 26, 2016 Volume 25, 2015 Volume 24, 2014 Volume 23, 2013 Volume 22, 2012 Volume 21, 2011 Volume 20, 2010 Volume 19, 2009 Volume 18, 2008 Volume 17, 2007 Volume 16, 2006 Volume 15, 2005 Volume 14, 2004 Volume 13, 2003 Volume 12, 2002 Volume 11, 2001 Volume 10, 2000 Volume 9, 1999 Volume 8, 1998 Volume 7, 1997 Volume 6, 1996 Volume 5, 1995 Volume 4, 1994

Critical Reviews™ in Eukaryotic Gene Expression

DOI: 10.1615/CritRevEukarGeneExpr.v17.i4.30
pages 281-293

Roles of Smad3 in TGF-β Signaling During Carcinogenesis

Caroline Millet
Laboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Building 37, Room 2056B, Bethesda, MD 20892-4256
Ying E. Zhang
Laboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Building 37, Room 2056B, Bethesda, MD 20892-4256

RESUMO

Signaling of transforming growth factor β (TGF-β) is mediated through a heteromeric complex of two types of transmembrane receptors and downstream intracellular proteins known as Smads. Alterations of TGF-β signaling underlie various forms of human cancer and developmental diseases. Human genetic studies have revealed both point mutations and deletions of Smad2 or Smad4 in several types of cancers. However, the role of Smad3 in tumorigenesis is not clear. Recent data indicate that Smad3 also functions as a tumor suppressor by inhibiting cell proliferation and promoting apoptosis. In addition, Smad3 is essential for TGF-β-mediated immune suppression, and it plays an important role in regulating transcriptional responses that are favorable to metastasis. Therefore, through regulating different transcriptional responses, Smad3 functions as both a negative and positive regulator of carcinogenesis depending on cell type and clinical stage of the tumor.


Articles with similar content:

Yin Yang 1 in Human Cancer
Critical Reviews™ in Oncogenesis, Vol.16, 2011, issue 3-4
Richard Byers, Khimara Naidoo, Sarah Nicholson, Helen Whitehouse
The Caspase-8 Modulator c-FLIP
Critical Reviews™ in Immunology, Vol.25, 2005, issue 1
Takao Kataoka
The Nuclear Matrix as a Target for Viral and Cellular Oncogenes
Critical Reviews™ in Eukaryotic Gene Expression, Vol.10, 2000, issue 1
Wolfgang Deppert
Gene Regulation Associated with Apoptosis
Critical Reviews™ in Eukaryotic Gene Expression, Vol.7, 1997, issue 1-2
Barbara A. Osborne, Birgit M. Jehn
Tyrosine Phosphorylation in Immune Cells: Direct and Indirect Effects on Toll-Like Receptor-Induced Proinflammatory Cytokine Production
Critical Reviews™ in Immunology, Vol.29, 2009, issue 4
Pauline Johnson, Jennifer L. Cross