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Updated: Jul 12, 2026

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
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Roles of Smad3 in TGF-beta signaling during carcinogenesis

Caroline Millet1, Ying E Zhang

  • 1Laboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Building 37, Room 2056B, Bethesda, MD 20892-4256, USA.

Critical Reviews in Eukaryotic Gene Expression
|August 30, 2007
PubMed

Insights

Transforming growth factor beta (TGF-beta) signaling involves Smad proteins. Smad3 acts as both a tumor suppressor and promoter, influencing cancer development and metastasis.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Signaling

Background:

  • Transforming growth factor beta (TGF-beta) signaling is crucial for cellular functions and is mediated by Smad proteins.
  • Dysregulation of TGF-beta signaling is implicated in various human cancers and developmental disorders.
  • While Smad2 and Smad4 alterations are linked to cancer, the specific role of Smad3 in tumorigenesis remains less understood.

Purpose of the Study:

  • To elucidate the multifaceted role of Smad3 in cancer development and progression.
  • To investigate Smad3's function as a tumor suppressor and its influence on metastasis.
  • To understand how Smad3 regulates transcriptional responses in different cellular contexts.

Main Methods:

  • Review of existing human genetic studies on Smad mutations in cancer.
  • Analysis of recent data on Smad3's function in cell proliferation and apoptosis.
  • Examination of Smad3's role in TGF-beta-mediated immune suppression and metastasis regulation.

Main Results:

  • Smad3 exhibits tumor suppressor activities by inhibiting cell proliferation and promoting apoptosis.
  • Smad3 is essential for TGF-beta-induced immune suppression.
  • Smad3 influences transcriptional responses that can either favor or inhibit metastasis.

Conclusions:

  • Smad3 plays a dual role in carcinogenesis, acting as both a negative and positive regulator.
  • The specific function of Smad3 depends on the cell type and the clinical stage of the tumor.
  • Further research into Smad3's complex regulatory mechanisms is warranted for cancer therapy.

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