Table 4.
M-MDSCs in cancer.
| Pro-Tumor Targeting in MDSCs | Cancer Type | Metabolic Regulation Mechanism | Ref. |
|---|---|---|---|
| mTOR | 3LL Lewis lung carcinoma | Tumor-infiltrating M-MDSCs are associated with increased glycolysis induced by mTOR and display strong inhibitory abilities | [49] |
| iNOS | Non-small cell lung cancer | MDSCs with high expression of iNOS inhibit T cell functions, which leads to poor response to chemotherapy | [114] |
| Ovarian cancer | Compared with healthy donors, the number of M-MDSCs increased in ovarian cancer, and the overexpression of iNOS was induced by STAT3 | [115] | |
| Prostate cancer | High levels of iNOS overexpressing MDSCs are positive correlated with the number of Tregs | [116] | |
| IDO | Gastric cancer | M-MDSCs (not PMN-MDSCs) produce IDO and blunt anti-tumor response of T cells | [117] |
| Chronic lymphocytic leukemia | M-MDSCs suppress the activity of T cells and induce Tregs by increasing IDO activity | [118] | |
| Melanoma | IDO was highly expressed in M-MDSCs rather than PMN-MDSCs, and the IDO activity is positively correlated with tumor growth | [119] | |
| CPT1 | Renal cell carcinoma; Breast cancer; Colon cancer | M-MDSCs inhibit immune response by increasing the expression of CPT1 and uptake of FA to promote FAO in tumor | [77] |
| mGluR2/3 | Melanoma | M-MDSCs promotes melanoma growth and inhibits the proliferation of T cells via metabotropic glutamate receptor (mGluR) 2/3 | [105] |