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. 2021 May 20;9:637675. doi: 10.3389/fcell.2021.637675

FIGURE 2.

FIGURE 2

Cancer-associated fibroblasts and drug resistance. The intricate mechanisms of drug resistance mediated by CAFs include secreting soluble factors, delivering exosomes, metabolic reprogramming and extracellular matrix (ECM) remodeling. CAFs can secret a broad range of cytokines or factors which enable to activate a series of signaling cascades, leading to therapeutic resistance. CAFs-derived exosomes deliver miRNAs, lncRNAs and mtDNA to cancer cells, which participate in transmitting paracrine signals of therapeutic resistance. Moreover, in order to adapt to a glucose-deficient microenvironment, CAFs coordinate with tumor cells to modulate metabolic mode. Lastly, activated signals within CAFs increased production of extracellular matrix components, resulting in changes of its physical and biochemical characteristics under therapeutic pressure. CCL1, chemokine C-C motif ligand-1; CCL5, chemokine C-C motif ligand-5; IL-6, interleukin-6; IL-8, interleukin-8;IL-11, interleukin-11; SDF1, stromal cell derived factor-1; HGF, hepatocyte growth factor; TGF-ß, transforming growth factor-β; IGF-2, insulin-like growth factor 2; PAI-1, plasminogen activator inhibitor-1, MMP, matrix metalloproteinase; HA, hyaluronan; HSPG2, heparin sulphate proteoglycan 2; LPP, lipoma-preferred partner. The figure was created with BioRender.com.