Related Experiment Video

Updated: Jun 30, 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

The YAP-TEAD4 inhibitor M511-0965 suppresses triple-negative breast cancer progression by downregulating TGFB2

Mengxing Cheng1, Xinyu Li1, Na Song1

  • 1Department of Pharmacology (State Key Laboratory of Frigid Zone Cardiovascular Diseases, State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin 150086, China.

Translational Oncology
|June 28, 2026
PubMed

Insights

Researchers identified a novel small-molecule inhibitor targeting TEAD4 to treat triple-negative breast cancer (TNBC). This YAP/TEAD4 inhibitor offers a promising, low-toxicity therapeutic strategy for TNBC, addressing unmet clinical needs.

Area of Science:

  • Oncology
  • Molecular Biology
  • Drug Discovery

Background:

  • Triple-negative breast cancer (TNBC) lacks targeted therapies, necessitating novel, low-toxicity treatments.
  • The Hippo pathway regulates organ development; its effector TEAD is implicated in various cancers.
  • TEAD4 is highly expressed in TNBC, influencing its biological functions and presenting a therapeutic target.

Purpose of the Study:

  • To identify safe and low-toxicity small-molecule inhibitors targeting TEAD4 for TNBC treatment.
  • To investigate the role of TEAD4 in TNBC progression and its potential as a therapeutic target.

Main Methods:

  • Bioinformatics and molecular biology experiments to analyze TEAD4 expression in TNBC.
  • Structure-based virtual screening using molecular docking to identify inhibitors of the YAP/TEAD4 complex.
  • In vitro molecular biology and cellular functional assays to validate inhibitor efficacy.

Main Results:

  • TEAD4 was found to be highly expressed in TNBC, correlating with tumor biological functions.
  • A novel small-molecule inhibitor targeting the YAP/TEAD4 interaction was identified through virtual screening.
  • The inhibitor demonstrated antitumor effects by disrupting the YAP/TEAD4 interaction in cellular assays.

Conclusions:

  • TEAD4 is a crucial therapeutic target in triple-negative breast cancer.
  • The identified small-molecule inhibitor targeting YAP/TEAD4 interaction shows preclinical promise for TNBC therapy.
  • This study provides a foundation for developing novel, low-toxicity targeted therapies for TNBC.
Keywords:
M511-0965Small molecule inhibitorTEAD4TGFB2TNBCVirtual screening

More Related Videos

Combined Use of Tail Vein Metastasis Assays and Real-Time In Vivo Imaging to Quantify Breast Cancer Metastatic Colonization and Burden in the Lungs10:32

Combined Use of Tail Vein Metastasis Assays and Real-Time In Vivo Imaging to Quantify Breast Cancer Metastatic Colonization and Burden in the Lungs

Published on: December 19, 2019

Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NFκB Activity and Breast Cancer Stem Cells13:38

Synthesis and Characterization of an Aspirin-fumarate Prodrug that Inhibits NFκB Activity and Breast Cancer Stem Cells

Published on: January 18, 2017

Related Concept Videos

TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR activation may...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...