fig2

Emerging roles of small extracellular vesicles in metabolic reprogramming and drug resistance in cancers

Figure 2. Lipid metabolic reprogramming regulates sensitivity to antitumor therapy. a: Fatty acid β-oxidation. b: De novo lipogenesis. c: Eicosanoid synthesis. d: Neutral lipolysis. e: Lipid ROS and ferroptosis. ACLY: ATP-citrate lyase; ACC1: acetyl-CoA carboxylase; FASN: fatty acid synthase; SCD: stearoyl-CoA desaturase; AMPK: adenosine 5’-monophosphate (AMP)-activated protein kinase; CPT: carnitine palmitoyl transferase; JNK: c-Jun N-terminal kinase; HER: human epidermal growth factor receptor; MAPK: mitogen-activated protein kinase; NF-κB: nuclear factor kappa-light-chain-enhancer of activated B cells; EGFR: epidermal growth factor receptor; AKT: protein kinase B; JAK2/STAT3: Janus kinase 2/signal transducer and activator of transcription 3; PI3K: phosphatidylinositol 3-kinase.

Cancer Drug Resistance
ISSN 2578-532X (Online)

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Portico

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