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Fig. 3 | Journal of Hematology & Oncology

Fig. 3

From: Crosstalk among m6A RNA methylation, hypoxia and metabolic reprogramming in TME: from immunosuppressive microenvironment to clinical application

Fig. 3

m6A methylation promotes immunosuppressive TME properties and supports tumor proliferation through pathways involving hypoxia, metabolic dysregulation, tumor exosomes and immune cells. HIF influences tumor cells under hypoxic conditions through m6A methylation modifications. Tumor cells in hypoxia accelerate the release of exosomes, contributing to the formation of immunosuppressive TME. m6A-mediated metabolic dysregulation generates an acidic environment that further supports tumor growth and exacerbates tumor hypoxia. A number of metabolites support immunosuppressive characteristics. In hypoxic conditions, tumors undergo metabolic reprogramming mediated by a HIF-induced positive feedback loop to further exacerbate metabolic dysregulation. Additionally, m6A methylation directly regulates immune cells to promote the progressive establishment of immunosuppressive TME

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