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Related Experiment Video

Updated: Jan 23, 2026

De Novo Generation of Somatic Stem Cells by YAP/TAZ

De Novo Generation of Somatic Stem Cells by YAP/TAZ

Published on: May 7, 2018

Basroparib inhibits YAP-driven cancers by stabilizing angiomotin.

Young-Ju Kwon^1,2, Dong Young Kim¹, Yuna Kim¹

¹Division of Radiation Biomedical Research, Korea Institute of Radiological and Medical Sciences, Seoul, Korea.

Molecular Oncology

|January 22, 2026

Summary

Basroparib, a tankyrase inhibitor, reduces cancer growth by stabilizing angiomotin (AMOT) to block the YAP oncogene. This drug overcomes resistance to MEK inhibitors in KRAS-mutant colorectal cancers.

Keywords:

MEK inhibitor resistance YAP angiomotin basroparib tankyrase inhibitor

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A Murine Cell Line Based Model of Chronic CDK9 Inhibition to Study Widespread Non-Genetic Transcriptional Elongation Defects TEdeff in Cancers

Published on: September 26, 2019

Area of Science:

Oncology
Molecular Biology
Drug Discovery

Background:

Yes-associated protein (YAP) is a critical oncogene and a major cause of resistance to cancer therapies, particularly in KRAS-mutant tumors.
Targeting YAP is clinically relevant, but direct inhibitors are scarce.
Tankyrase (TNKS) inhibitors, like basroparib, suppress Wnt signaling and may offer an indirect approach to YAP inhibition.

Purpose of the Study:

To investigate the efficacy of basroparib in attenuating YAP-driven oncogenic programs.
To determine if basroparib can overcome resistance to MEK inhibitors in colorectal cancer (CRC).
To explore basroparib's potential as a dual Wnt-YAP pathway inhibitor.

Main Methods:

Treatment of colorectal cancer cells with basroparib.
Assessment of angiomotin (AMOT) protein levels and AMOT-YAP complex formation.
Analysis of YAP localization and YAP-dependent transcription.
Evaluation of drug sensitivity to MEK inhibitors in YAP-overexpressing and MEK inhibitor-resistant CRC models.
In vitro and in vivo studies in various YAP-active tumor models.

Main Results:

Basroparib increased AMOT protein, promoted AMOT-YAP complex formation, and led to YAP cytoplasmic sequestration, reducing YAP transcription.
Basroparib sensitized YAP-overexpressing, KRAS-mutant CRC cells to MEK inhibition.
In MEK inhibitor-resistant CRC models, basroparib restored sensitivity to MEK inhibitors.
The drug enhanced MEK inhibitor efficacy in other YAP-active tumors but not in YAP-inactive models.

Conclusions:

Basroparib effectively inhibits YAP-driven oncogenic programs by stabilizing AMOT.
Basroparib shows promise in overcoming therapeutic resistance in YAP-driven cancers, particularly KRAS-mutant CRC.
Basroparib represents a potential therapeutic strategy for dual Wnt-YAP pathway blockade and warrants further clinical investigation (Phase I, NCT04505839).