Fig. 9

A proposed model illustrating how CAFs drive a more aggressive phenotype in BC by recruiting monocytes in a paracrine manner. CAFs contribute to preparing an immunosuppressive TME by recruiting monocytes and educating them into a distinct population of macrophages exhibiting an M2-like phenotype. As a plausible mechanism, exosomal transfer of miR-181a from CAF-educated monocytes is partly associated with activating Akt signaling and up-regulating EMT markers, thereby promoting breast tumor progression and growth