Fig. 6
From: Mitochondrial metabolism and cancer therapeutic innovation
Mitochondria-mediated crosstalk in the tumor microenvironment. Mitochondrial interactions drive complex cellular dynamics within the tumor microenvironment. Immune cells such as cytotoxic T lymphocytes, natural killer cells, and M1 macrophages generate antitumor responses through reactive oxygen species and inflammatory signals. Conversely, immunosuppressive cells such as regulatory T cells and M2 macrophages promote tumor survival by secreting growth factors. Cancer-associated fibroblasts support tumor progression through metabolic resources and signaling molecules. Tumor cells adapt by modifying mitochondrial function, enhancing metabolic flexibility, and establishing intricate communication networks that ultimately facilitate tumor survival, angiogenesis, and resistance to therapeutic interventions. The mitochondria depicted in this figure are derived from cancer cells. CTLs cytotoxic T cells, CAFs cancer-associated fibroblasts, Cyt c cytochrome c, ETC electron transport chain, EVs extracellular vesicles, GLUT1 glucose transporter 1, HIF-1α hypoxia-inducible factor 1-alpha, IFN-γ interferon-gamma, IL-1β interleukin 1 beta, IL-6/10 interleukin 6/10, IRF1 interferon regulatory factor 1, MFN1/2 mitofusin 1/2, MOMP mitochondrial outer membrane permeabilization, NETs neutrophil extracellular traps, NO nitric oxide, Nrf2 nuclear factor erythroid 2-related factor 2, OXPHOS oxidative phosphorylation, PHD prolyl hydroxylase domain, ROS reactive oxygen species, TGF-β transforming growth factor-beta, TNTs tunneling nanotubes, TNF-α tumor necrosis factor-alpha, VEGF vascular endothelial growth factor. This figure was created with BioRender (https://biorender.com/)
