Fig. 4

The regulation and the oncogenic roles of ERO1α on tumors. For the regulation of ERO1α, only hypoxia is shown in this figure. In the TME, hypoxia enhances ERO1α via up-regulating HIF-1α. ERO1α not only endows tumor cells with an aggressive phenotype and promotes aerobic glycolysis of tumor cells, but also contributes to induce an immunosuppressive TME by activating immunosuppressive cells while inhibiting immunocompetent cells. ERO1α, endoplasmic reticulum oxidoreductase 1 alpha; PDI, protein disulfide isomerase; EMT, epithelial-mesenchymal transition; VEGF, vascular endothelial growth factor; MMP, matrix degrading enzyme; ECM, extracellular matrix; MDSC, myeloid-derived suppressor cell; G-CSF, granulocyte colony-stimulating factor; CXCL1/2, C-X-C motif chemokine ligand 1/2. PD-L1, programmed cell death ligand-1