Cancer-associated fibroblast activation (CAF)

Cancer-associated fibroblast activation is not a discrete molecular target but describes a collective change in stromal cell phenotype. Activated CAFs promote tumor growth by remodeling the tumor microenvironment, secreting angiogenic and immunosuppressive factors, and undergoing metabolic shifts (such as the reverse Warburg effect) that support cancer cell metabolism[1][3][7][8]. CAF activation is regulated by signals from cancer cells, immune cells, and other local or systemic factors (including TGF-β, IL-1, and hypoxia), and is associated with markers such as α-SMA and FAP[1][7]. The diverse roles and heterogeneity of CAFs have made them an area of intense research for therapeutic strategies aimed at disrupting tumor–stroma interactions[5][7]. However, “fibroblast activation” itself is a process, not a singular druggable protein, so it is not considered a canonical molecular target.\nThe term “cancer-associated fibroblast activation” is *not* a canonical target (such as a receptor or enzyme), but rather a cellular state/process. Research focuses on blocking this process by targeting its mediators (FAP, TGF-β pathways, etc.) or functional consequences (ECM remodeling, immune suppression)[1][5][7][8].\nIf you need information about a specific marker or molecule within this context (e.g., Fibroblast activation protein [FAP]), that would be considered a therapeutic target and could be detailed with structured information.

Other names

Tumor-associated fibroblastcarcinogenic-associated fibroblastactivated fibroblast

Inhibition of CAF-mediated signaling, blocking growth factor or cytokine signaling, ECM modulation, depletion of CAF populations, interference with metabolic crosstalk