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Fig. 2 | Cancer Communications

Fig. 2

From: When fats commit crimes: fatty acid metabolism, cancer stemness and therapeutic resistance

Fig. 2

Potential roles of fatty acid metabolism in regulating cancer cell plasticity. Cancer cells can be reprogrammed into a cancer stemness state or drug-tolerant state with appropriate cues. It has been shown that adipocytes in the tumor microenvironment secrete leptin, transforming growth factor β (TGFβ) or other hormones and growth factors that support conversion of cancer cells into more malignant cell types, including cancer stem cells/tumor-initiating cells or drug-tolerant persisters. Acetyl-CoA is a central hub for multiple metabolic pathways including FA synthesis and FAO. Therefore, acetyl-CoA might be a major carbon source for histone acetylation and regulating gene expression for reprogramming. ACSS2 is phosphorylated and transferred to nucleus for histone acetylation. Some transcription factors, including hypoxia inducible factor-1α (HIF-1α), signal transducer and activator of transcription 3 (STAT3) and SMAD family member 2 (Smad2), are also involved in the conversion and may drive cancer cell plasticity

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