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. 2021 Jul 29;46(3):208. doi: 10.3892/or.2021.8159

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Copyright: © Liang et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 3. — Regulation of ROS in tumor cell metabolism. Specifically, metabolic alterations in cancer cells cause the accumulation of ROS, which in turn acts on metabolic enzymes to promote the metabolic programming of cancer cells. The accumulation of ROS can also activate CAFs and promote autophagy, which can further increase the accumulation of ROS and provide raw materials for tumor metabolism. In addition, ROS are also involved in the inhibition of T cell function by tumor metabolism. CAFs, carcinoma associated fibroblasts; Cav-1, caveolin-1; CXCL12, chemokine (C-X-C motif) ligand 12; ER, endoplasmic reticulum; HIF-1, hypoxia inducible factor 1; Mito-ETC, mitochondrial electron transport chain; NOXS, NADPH oxidases; ROS, reactive oxygen species.