Breast cancer progression is promoted by both local inflammation and fibrosis. Indeed,accumulation of fibrous collagen is an independent prognosis marker of breast cancer. However, the mechanisms underlying the interplay between fibroblasts, inflammation and tumor progression remain unclear. Our early observations highlighted a potential role of inflammasome activation in cancer associated fibroblasts in both local inflammation and fibrous collagen accumulation. Thus, in the L929 in vitro fibroblast model, we investigated whether inflammasome activation led to a cancer- associated fibroblast phenotype and whether such phenotype promoted pro- inflammatory cytokine release and/or fibrous collagen secretions. Our data indicate that activation of fibroblasts was associated with promotion of inflammasome especially NLPR3 inflammasome activation. Moreover, inflammasome activation was associated with a cancer- associated fibroblast (CAF) phenotype as demonstrated by increases in alpha smooth actin and vimentin expression. In addition, incubation with the NF-kB inhibitor MG132 underlined the critical role of NF-kB in the secretion of fibrous collagen. Our observations regarding the potential of the gasdermin inhibitor Disulfiram (DS) to alone prevent inflammasome driven activities were unconclusive. Interestingly, the NLRP3 inflammasome specific inhibitor, MCC950 altered both the expression and secretion of pro-inflammatory cytokines. With regard to fibrosis and collagen accumulation, blocking the NF-KB or the inflammasome activation but not the gasdermin D cleavage drastically altered the CAF phenotype in particular with regard to collagen subtype secreted and cytokines produced. Moreover, combination of MG132 and MCC950 reverted CAF phenotype and limited both pro- inflammatory cytokine secretion as well as fibrous collagen secretions. Taken together our data suggest that L929 fibroblasts model CAFs in vitro and that fibrosis is in part triggered by NLRP3 inflammasome activation, and also actively involve the NF-kB signaling pathway. Future investigations will aim to further those observations and possibility target those pathways in stroma cells to prevent/limit breast cancer progression.