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Updated: Jan 20, 2026

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
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Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

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Identification of novel TGF-β regulated genes with pro-migratory roles

Qi Liu1, Nicholas Borcherding2, Peng Shao1

  • 1Department of Anatomy and Cell Biology, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.

Biochimica Et Biophysica Acta. Molecular Basis of Disease
|August 27, 2019
PubMed

Insights

Transforming growth factor-beta (TGF-β) signaling impacts cell development and cancer. This study used RNA-sequencing to identify novel genes and epigenetic mechanisms, like KDM7A, involved in TGF-β-driven cell migration and cancer progression.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Transforming growth factor-beta (TGF-β) signaling is crucial for cell development and homeostasis.
  • Dysregulated TGF-β signaling contributes to cancer progression, epithelial-to-mesenchymal transition (EMT), cancer stem cell enrichment, and immunosuppression.
  • Limited next-generation sequencing datasets exist for TGF-β-regulated genes.

Purpose of the Study:

  • To identify novel genes and pathways regulated by TGF-β using RNA-sequencing.
  • To investigate the role of identified genes and epigenetic modifications in TGF-β-induced cell migration.
  • To explore the potential of these findings in understanding cancer progression and therapeutic relapse.

Main Methods:

  • RNA-sequencing analysis of MCF10A cells treated with TGF-β.
  • Gene set enrichment analysis to identify enriched pathways.
  • Confirmation of gene expression and functional assays for cell migration.
  • Analysis of epigenetic modifications, specifically H3K27 acetylation.

Main Results:

  • Identified 1166 upregulated and 861 downregulated genes in response to TGF-β.
  • Focal adhesion and metabolic pathways were top enriched pathways for up- and downregulated genes, respectively.
  • TGF-β induced expression of MICAL1, MICAL2, and KDM7A, which regulate cell migration.
  • KDM7A critically affects H3K27 acetylation on TGF-β-induced genes.

Conclusions:

  • This study identified novel effectors, including MICAL family members and KDM7A, mediating TGF-β's pro-migratory role.
  • Revealed novel epigenetic mechanisms, specifically KDM7A's role in H3K27 acetylation, downstream of TGF-β signaling.
  • These findings provide a basis for future research into MICAL family functions in cancer and TGF-β-mediated epigenetic regulation.
Keywords:
EpigeneticsKDM7A/JHDM1DMICAL1MigrationTGF-β

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