MRC2 (Mannose Receptor C Type 2)

Further, we find that MRC2 is functional on AML cells, and enables their robust uptake of collagen, which supports their glycolytic metabolism. In sum these data highlight the use of functional surface markers to distinguish LSC in AML, and how they can yield insight into their unique characteristics.

Our results suggest that MRC2 could be used as a novel prognostic marker and therapeutic target for HNSCC.

In conclusion, this study identified a novel approach for suppressing osteosarcoma proliferation. Reduction of MRC2 activity inhibits osteosarcoma proliferation in patients with high MST4 expression by altering the cell cycle, which may be valuable for treating osteosarcoma and improving patient prognosis.

Altogether, our data propose MRC2 as a new LSC marker that potently regulates the interaction of LSCs with their microenvironment. Mechanisms by which MRC2 expression is modulated are likely to be responsible for AML heterogeneity and plasticity and has new implications for LSC identification.

The immunotherapeutic response prediction was performed in two independent cohorts (GSE78220: metastatic melanoma with pembrolizumab treatment and IMvigor210: advanced urothelial cancer with atezolizumab intervention). This study demonstrated that MRC2 could be a prognostic indicator for certain cancer and is critical for tumor immune microenvironments. MRC2 expression level may influence and predict immune checkpoint blockade response as a potential indicator.

Addition of wild-type, but not Endo180-deficient, CAFs in co-implantation studies restricted CD8+ T cell intratumoral infiltration, and tumors in Endo180 knockout mice exhibited increased CD8+ T cell infiltration and enhanced sensitivity to ICB compared to tumors in wild-type mice. Clinically, in a trial of melanoma patients, high MRC2 mRNA levels in tumors was associated with a poor response to αPD-1 therapy, highlighting the potential benefits of therapeutically targeting a specific CAF subpopulation in breast and other CAF-rich cancers to improve clinical responses to immunotherapy.