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Updated: Aug 28, 2025

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

Published on: October 27, 2020

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TGFB2-AS1 inhibits triple-negative breast cancer progression via interaction with SMARCA4 and regulating its targets

Cixiang Zhou1, Difei Wang1, Jingchi Li1

  • 1State Key Lab of Oncogene and Related Genes, Renji Hospital, Shanghai Institute of Cancer, Key Lab of Cell Differentiation and Apoptosis of Ministry of Education, Research Unit 2019RU043, Chinese Academy of Medical Sciences, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.

Proceedings of the National Academy of Sciences of the United States of America
|September 20, 2022
PubMed

Insights

This study identifies the long noncoding RNA TGFB2-AS1 as a key regulator in triple-negative breast cancer (TNBC). TGFB2-AS1 inhibits cancer stem cell traits, reducing metastasis and improving patient outcomes.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Triple-negative breast cancer (TNBC) presents significant challenges due to high relapse rates, metastatic potential, and poor survival.
  • The mechanisms by which non-stem cancer cells gain stem-cell properties and contribute to metastasis are not well understood.

Purpose of the Study:

  • To identify regulators of plasticity in non-stem cell populations within TNBC.
  • To investigate the role of long noncoding RNA TGFB2-AS1 in TNBC progression and metastasis.

Main Methods:

  • In vitro and in vivo experiments using TNBC cell lines and mouse models.
  • Analysis of TGFB2-AS1 interaction with SMARCA4 and its effect on target gene transcription.
  • Correlation analysis of TGFB2-AS1 and TGFβ2 expression with patient prognosis.

Main Results:

  • TGFB2-AS1 was identified as a regulator that impairs breast cancer stem-like cell (BCSC) traits in TNBC.
  • TGFB2-AS1 significantly reduced tumor formation and lung metastasis in vivo.
  • TGFB2-AS1 interacts with SMARCA4 to transcriptionally repress TGFB2 and SOX2, inhibiting TGFβ signaling and BCSC characteristics.
  • Overexpression of TGFB2-AS1 abrogated TGFβ2-enhanced tumor growth and metastasis.
  • High TGFB2-AS1 and low TGFβ2 levels correlated with better patient outcomes.

Conclusions:

  • TGFB2-AS1 plays a crucial role in inhibiting TNBC progression by modulating cancer cell fate and plasticity.
  • TGFB2-AS1 acts as a tumor suppressor by reducing stem-like properties and metastatic potential.
  • These findings offer potential therapeutic strategies targeting TGFB2-AS1 for TNBC treatment.
Keywords:
SWI/SNF complexTGFB2-AS1TGFβ signalingcancer stem-like celltriple-negative breast cancer

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