Fig. 2
From: Molecular mechanisms of tumor resistance to radiotherapy
The development of radioresistance in the tumor microenvironment after radiation. Radiation can induce hypoxia, fibrosis, vascular damage, chronic inflammation, and immunosuppression in the tumor microenvironment, all of which may lead to RT resistance. Cancer-associated fibroblasts are also important aspects of the tumor microenvironment for the generation of radioresistance because they affect immune cells in such a way that leads to immunosuppression, fibrosis, and extracellular matrix remodeling. RT: radiation therapy, ROS: reactive oxygen species, GSH: glutathione, VEGF: vascular endothelial growth factor, Treg: regulatory T cells, NK: natural killer cells, DC: dendritic cells, CAF: tumor-associated fibroblasts, MDSCs: bone-marrow-derived suppressor cells, ECM: extracellular matrix, IL-1α: interleukin-1α, HIF-1α: hypoxia-inducible factor 1α, PDGF: Platelet-derived growth factor, CSC: Cancer stem cell, NADPH: nicotinamide adenine dinucleotide phosphate oxidase, TGF-β: transforming growth factor-β, CHK1: checkpoint kinase 1, CHK2: checkpoint kinase 2, cGAS: cyclic GMP-AMP synthase, STING: stimulator of interferon genes, IFN: interferon, PD‑L1: programmed cell death 1 ligand 1, IL‑10: interleukin 10, ICD: immunogenic cell death