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. Author manuscript; available in PMC: 2025 Jul 23.
Published in final edited form as: Physiol Rev. 2025 Jan 15;105(3):1291–1428. doi: 10.1152/physrev.00034.2023

Figure 11. Salient non-myeloid NOX signaling pathways in cancer development and progression.

Figure 11.

Non-myeloid NOX2-derived ROS may facilitate cancer expansion by promotion of cell proliferation and a phenomenon described as “apoptotic escape”; ROS can evoke the capacity to redirect osteosarcoma from programmed death to survival. Adaptor Hic-5, which reportedly suppresses NOX4, is downregulated in metastatic cancer cells and unleashes NOX4-mediated invasiveness. NOX4-derived H2O2 causes oxidation of CR1 in BRAF propagating exaggerated NRAS-mediated MEK and ERK activation, and melanoma progression. NOX4 overexpression is linked to EMT and invasion via JAK2/STAT3. DUOX2 is implicated in PKC-induced Akt/MAPK activation and proliferation, migration, and invasion in colon cancer. NOX1 via MAPK induces cyclin D1 and proliferation as well as activates ADAM17-EGFR-PI3K-Akt signaling and increases the expansion of colon cancer cells.