Inhibition of RAC1 activity in cancer associated fibroblasts favours breast tumour development through IL-1β upregulation

Cancer-associated fibroblasts (CAFs) are highly abundant stromal components in the tumour microenvironment. These cells contribute to tumorigenesis and indeed, they have been proposed as a target for anti-cancer therapies. Similarly, targeting Rho-GTPase RAC1 has also suggested potential therapeutic cancer. Here, we show that activity, either pharmacologically or by genetic silencing, increases pro-tumorigenic activity of CAFs upregulating IL-1β secretion. Moreover, inhibiting shifts CAF subtype more aggressive phenotype. Thus, suppresses secretion CAFs, reducing combination with depletion this cytokine should be considered an interesting option breast cancer which retain intact signalling.