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Updated: May 10, 2026

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
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MiR-21/Smad 7 signaling determines TGF-β1-induced CAF formation

Qiong Li1, Daoxiang Zhang, Yongbin Wang

  • 1Department of Biochemistry & Molecular Cell Biology, Shanghai Key Laboratory of Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine.

Scientific Reports
|June 21, 2013
PubMed

Insights

MicroRNA-21 (miR-21) and its target, Smad 7, regulate the formation of carcinoma-associated fibroblasts (CAFs) by controlling transforming growth factor-beta 1 (TGF-β1) signaling.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • Carcinoma-associated fibroblasts (CAFs) play a crucial role in tumor progression.
  • The precise mechanisms regulating TGF-β1-induced CAF generation are not fully understood.

Purpose of the Study:

  • To elucidate the role of miR-21 and its target Smad 7 in TGF-β1-mediated CAF formation.

Main Methods:

  • Primary human fibroblasts were treated with TGF-β1.
  • miR-21 and Smad 7 levels were analyzed.
  • miR-21's interaction with Smad7 mRNA was investigated.
  • Functional studies involved miR-21 or Smad 7 depletion/overexpression.

Main Results:

  • TGF-β1 treatment increased mature miR-21 and decreased Smad 7 protein levels in fibroblasts.
  • miR-21 directly inhibits Smad 7 translation by binding to its 3' UTR.
  • Smad 7 negatively regulates TGF-β1 signaling by interfering with Smad 2/3 activation.
  • Modulating miR-21 or Smad 7 levels significantly impacted CAF formation.

Conclusions:

  • miR-21 and Smad 7 are key regulators of TGF-β1 signaling in CAF induction.
  • This pathway represents a potential therapeutic target for cancer treatment.

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