fig1
Figure 1. Mechanisms by which EVs regulate tumor drug resistance involving multiple factors and pathways[12]. EVs: Extracellular vesicles; CAFs: cancer-associated fibroblasts; miR: microRNA; circRNA: circular RNA; ciRS-122: circular RNA sponge for miR-122; circUHRF1: circular RNA UHRF1; CIRCUSP7: circular RNA USP7; Linc00852: long intergenic non-protein coding RNA 852; NF-κB: nuclear factor kappa-B; EGFR: epidermal growth factor receptor; PKM2: pyruvate kinase M2; PTEN: phosphatase and tensin homolog; Wnt: wingless-related integration site signaling pathway; β-catenin: beta-catenin; COMMD7: copper metabolism MURR1 domain-containing protein 7; ATP: adenosine triphosphate; ADP: adenosine diphosphate; NAD+: nicotinamide adenine dinucleotide (oxidized form); NADH: nicotinamide adenine dinucleotide (reduced form); Fe: iron.
