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Updated: Feb 21, 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

Published on: October 27, 2020

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GTSE1: a novel TEAD4-E2F1 target gene involved in cell protrusions formation in triple-negative breast cancer cell

Debora Stelitano1, Leticia Yamila Peche1, Emiliano Dalla1

  • 1Laboratorio Nazionale del Consorzio Interuniversitario per le Biotecnologie (L.N.CIB), Trieste, Italy.

Oncotarget
|October 6, 2017
PubMed

Insights

GTSE1 promotes metastasis in breast cancer by regulating cell migration via the TEAD4 pathway. Targeting pRb-E2F1 or YAP/TAZ-TEAD pathways may offer new treatments for triple-negative breast cancer (TNBC).

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • GTSE1 overexpression is linked to metastasis in various cancers, including breast cancer.
  • The transcriptional regulation and functional mechanisms of GTSE1 in tumors are poorly understood.
  • Triple-negative breast cancer (TNBC) presents a significant clinical challenge.

Purpose of the Study:

  • To investigate the transcriptional regulation of GTSE1.
  • To elucidate the role of GTSE1 in cell functions within TNBC.
  • To identify potential therapeutic targets for TNBC treatment.

Main Methods:

  • Identified GTSE1 as a target gene of the TEAD4 transcription factor.
  • Investigated the involvement of YAP and TAZ coactivators in GTSE1 regulation.
  • Analyzed the pRb-E2F1 pathway's role in GTSE1 transcription.
  • Evaluated the effects of targeting pRb-E2F1 and YAP/TAZ-TEAD pathways on gene expression.

Main Results:

  • GTSE1 is transcriptionally regulated by TEAD4, YAP, and TAZ.
  • TEAD4-mediated GTSE1 expression controls cell protrusions and migration.
  • The pRb-E2F1 pathway also regulates GTSE1 transcription.
  • Targeting pRb-E2F1 or YAP/TAZ-TEAD pathways downregulated GTSE1 and metastasis-associated genes.

Conclusions:

  • GTSE1 is a key effector in TEAD4-driven cell functions, promoting invasion and metastasis in breast cancer.
  • The pRb-E2F1 and YAP/TAZ-TEAD pathways are crucial regulators of GTSE1.
  • Therapeutic strategies targeting these pathways show promise for TNBC treatment.
Keywords:
E2F1GTSE1TEAD4YAP/TAZcell protrusions

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