Integration of focal adhesion morphogenesis and polarity by DOCK5 promotes YAP/TAZ-driven drug resistance in TNBC.

ABSTRACT: YAP and TAZ are transcriptional co-activators that are inhibited by sequestration in the cytoplasm. Cellular signalling pathways integrate soluble, mechanical (cytoskeleton, adhesion), and geometric (cell size, morphology) cues to regulate the translocation of YAP/TAZ to the nucleus. In triple-negative breast cancer (TNBC) cells, both signalling and morphogenesis are frequently rewired, leading to increased YAP/TAZ translocation, which drives proliferation, invasion, and drug resistance. However, whether this increased YAP/TAZ translocation is due to alterations in upstream signalling events or changes in cell morphology remains unclear. To gain insight into YAP/TAZ regulation in TNBC cells, we performed multiplexed quantitative genetic screens for YAP/TAZ localisation and cell shape, enab

SUBMITTER: Pascual-Vargas P 

PROVIDER: S-EPMC12068046 | biostudies-literature | 2025 May

REPOSITORIES: biostudies-literature