Endoglin mediates the tumor- and metastasis-promoting traits of stromal myofibroblasts in human breast carcinomas.

ABSTRACT: Carcinoma-associated fibroblasts (CAFs), which are abundant in the tumor microenvironment, influence cancer hallmarks. We previously described transforming growth factor-β (TGF-β)-Smad2/3 signaling as being activated in myofibroblastic CAFs (myCAFs) in an autocrine fashion by increasing TGF-β production. However, factors regulating such autocrine TGF-β signaling remain poorly understood. Herein, we show that the abundance of endoglin (ENG), a TGF-β superfamily coreceptor expressed on human breast myCAFs, is significantly associated with poorer outcomes of breast cancer patients. Inhibition of ENG expression on myCAFs not only suppressed the TGF-β-Smad2/3 pathway and TGF-β1 expression but also attenuated the ability of myCAF to promote primary tumor growth and metastasis. Mechanistically, E

SUBMITTER: Okubo S 

PROVIDER: S-EPMC12420333 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature