Our findings indicate that hMENA overexpression in CAFs defines a myofibroblast-like subset predominantly driven by TGF-β signaling, which sustains TGF-β1-mediated crosstalk between cancer cells and CAFs and impairs T-cell functionality. In NSCLC tissues, hMENAhigh CAFs associate with TGF-β and regulatory T-cell signatures and correlate with poor patient prognosis and resistance to immune checkpoint therapies, supporting their role as key contributors to an immunosuppressive, ICT-refractory tumor microenvironment.
Melchionna et al. (Thu,) studied this question.