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ERO1α-mediated immunosuppressive mechanism in the tumor microenvironment. Upregulation of ERO1α in cancer cells enhances the secretion of pro-inflammatory cytokines and chemokines such as G-CS), CXCL1, and CXCL2, which promote the recruitment and expansion of polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs). Simultaneously, ERO1α upregulates PD-L1 expression, further suppressing T cell-mediated anti-tumor immunity.

Journal: International Journal of Molecular Sciences

Article Title: ERO1α as a Potential Drug Target for Breast Cancer: A Systematic Review of Current Evidence

doi: 10.3390/ijms262110276

Figure Lengend Snippet: ERO1α-mediated immunosuppressive mechanism in the tumor microenvironment. Upregulation of ERO1α in cancer cells enhances the secretion of pro-inflammatory cytokines and chemokines such as G-CS), CXCL1, and CXCL2, which promote the recruitment and expansion of polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs). Simultaneously, ERO1α upregulates PD-L1 expression, further suppressing T cell-mediated anti-tumor immunity.

Article Snippet: 5 , 2019 , Takei et al. [ ] , ERO1α is a novel endogenous marker of hypoxia in human cancer cell lines , human, mice , MDA-MB-231 MCF7 , Under normoxic conditions, ERO1α is expressed across all tested cell lines, with notably higher levels in cancer cell lines. Additionally, the hypoxia marker CA9 is significantly elevated in the aggressive MDA-MB-231 breast cancer cells compared to both normal cells and MCF7 cells..

Techniques: Derivative Assay, Expressing