Cancerâassociated fibroblasts (CAFs) are a heterogeneous population of activated fibroblasts that constitute a dominant cellular component of the tumor microenvironment (TME) performing distinct functions. Here, the role of tumorâderived exosomes (Exos) in activating quiescent fibroblasts into distinct functional subtypes is investigated. Proteomic profiling and functional dissection reveal that earlyâ (SW480) and lateâstage (SW620) colorectal cancer (CRC) cellâderived Exos both activated normal quiescent fibroblasts (αâSMAâ, CAV+, FAP+, VIM+) into CAFâlike fibroblasts (αâSMA+, CAVâ, FAP+, VIM+). Fibroblasts activated by earlyâstage cancerâexosomes (SW480âExos) are highly proâproliferative and proâangiogenic and display elevated expression of proâangiogenic (IL8, RAB10, NDRG1) and proâproliferative (SA1008, FFPS) proteins. In contrast, fibroblasts activated by lateâstage cancerâexosomes (SW620âExos) display a striking ability to invade through extracellular matrix through upregulation of proâinvasive regulators of membrane protrusion (PDLIM1, MYO1B) and matrixâremodeling proteins (MMP11, EMMPRIN, ADAM10). Conserved features of Exosâmediated fibroblast activation include enhanced ECM secretion (COL1A1, TenascinâC/X), oncogenic transformation, and metabolic reprogramming (downregulation of CAVâ1, upregulation of glycogen metabolism (GAA), amino acid biosynthesis (SHMT2, IDH2) and membrane transporters of glucose (GLUT1), lactate (MCT4), and amino acids (SLC1A5/3A5)). This study highlights the role of primary and metastatic CRC tumorâderived Exos in generating phenotypically and functionally distinct subsets of CAFs that may facilitate tumor progression.