Related Experiment Video

Updated: Feb 6, 2026

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
06:54

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

Published on: October 27, 2020

14.4K

Function of GCN5 in the TGF-β1-induced epithelial-to-mesenchymal transition in breast cancer

Liming Zhao1, Aixia Pang2, Yunchun Li3

  • 1Department of Nuclear Medicine, Linyi People's Hospital, Linyi, Shandong 276000, P.R. China.

Oncology Letters
|August 22, 2018
PubMed

Insights

Histone acetyltransferase GCN5 promotes breast cancer progression by regulating epithelial-mesenchymal transition (EMT). Inhibiting GCN5 reduces cancer cell viability, migration, and invasion, suggesting GCN5 as a therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Histone acetyltransferase GCN5 (GCN5) is implicated in the TGF-β/Smad signaling pathway in breast cancer.
  • The specific role of GCN5 in breast cancer development and progression remains unclear.

Purpose of the Study:

  • To investigate the role of GCN5 in TGF-β1-induced epithelial-mesenchymal transition (EMT) in breast cancer cells.
  • To elucidate the molecular mechanisms underlying GCN5's function in breast cancer progression.

Main Methods:

  • Stimulation of MDA-MB231 breast cancer cells with TGF-β1.
  • GCN5 knockdown using specific siRNAs.
  • Analysis of EMT markers (E-cadherin, N-cadherin, vimentin, snail, slug).
  • Assessment of cell viability, migration, invasion, and key signaling molecules (p-STAT3, p-AKT, MMP9, E2F1, p21).

Main Results:

  • TGF-β1 stimulation increased GCN5 activity, mRNA, and protein expression in MDA-MB231 cells.
  • TGF-β1 induced EMT, decreasing E-cadherin and increasing mesenchymal markers; these effects were reversed by GCN5 knockdown.
  • GCN5 knockdown inhibited cell viability, migration, and invasion, and altered the expression of STAT3, AKT, MMP9, E2F1, and p21.

Conclusions:

  • GCN5 plays a crucial role downstream of the TGF-β/Smad signaling pathway in regulating EMT in breast cancer.
  • GCN5 inhibition suppresses breast cancer cell progression, highlighting its potential as a therapeutic target.
Keywords:
MDA-MB231breast cancerepithelial-mesenchymal-transitionhistone acetyltransferase GCN5transforming growth factor-β1

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