LATS1/2 Inactivation in the Mammary Epithelium Drives the Evolution of a Tumor-Associated Niche

ABSTRACT: Basal-like breast cancers exhibit distinct cellular heterogeneity that contributes to disease pathology. In this study we used a genetic mouse model of basal-like breast cancer driven by epithelial-specific inactivation of the Hippo pathway-regulating LATS1 and LATS2 kinases to elucidate epithelial-stromal interactions. We demonstrate that basal-like carcinoma initiation is accompanied by the accumulation of distinct cancer-associated fibroblast and macrophage recruitment, and dramatic extracellular matrix remodeling, phenocopying the stromal diversity observed in human triple-negative breast tumors. Dysregulated epithelial-stromal signals were observed, including those mediated by TGF-β, PDGF, and CSF. Autonomous activation of the transcriptional effector TAZ was observed in LATS1/2-delet

SUBMITTER: Joseph, G. Kern 

PROVIDER: S-SCDT-10_1038-S44319-025-00370-3 | biostudies-other |

REPOSITORIES: biostudies-other