Cancer-associated fibroblasts crosstalk with cancer cells under inflammation and stress. (IMAGE)
Caption
Cancer -CAF Interactions in metabolism:
(a) Inflammation: Cancer NF-κB with P53 mutation triggers TNF-α and IL-1 release, activating CAF NF-κB to produce IL-6. TNF-α aids IL-6 uptake by cancer and CAFs, activating STAT3 for proliferation. Direct FAP-integrin contact between CAFs and cancer cells also activates NF-κB, exacerbating inflammation.
(b)hypoxic and aerobic area: Glucose: Under oxidative stress, CAF autophagy downregulates Cav-1, enhancing oxidative stress and activating NF-κB to inhibit OXPHOS and boost glycolysis. Cancer cells in aerobic zones use lactic acid from CAFs to enhance OXPHOS, while hypoxic cancer cells produce lactic acid for aerobic cancer cells' energy needs. Protein: Cancer cells autophagically use exogenous glutamine to produce ammonia, inhibiting CAF mitochondrial function and enhancing autophagy. CAFs release their own glutamine for cancer cell uptake, activating cancer cell mitochondrial activity and metabolism.
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Tianlin He
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