MicroRNA-22 represses glioma development via activation of macrophage-mediated innate and adaptive immune responses

Macrophage-mediated tumor cell phagocytosis and subsequent neoantigen presentation are critical for generating anti-tumor immunity. This study aimed to uncover the potential clinical value and molecular mechanisms of miRNA-22 (miR-22) in tumor cell phagocytosis via macrophages and more efficient T cell priming. We found that miR-22 expression was markedly downregulated in primary macrophages from glioma tissue samples compared to adjacent tissues. miR-22-overexpressing macrophages inhibited glioma cell proliferation and migration, respectively. miR-22 upregulation stimulated the phagocytic ability of macrophages, enhanced tumor cell phagocytosis, antigen presentation, and efficient T cell priming. Additionally, our data revealed that miR-22-overexpressing macrophages inhibited glioma formation in vivo, HDAC6 was a target, and NF-kappa B signaling was a pathway closely associated with miR-22 in tumor-associated macrophages (TAMs) of glioma. Our findings revealed the essential roles of miR-22 in tumor cell phagocytosis by macrophages and more efficient T cell priming, facilitating further research on phagocytic regulation to enhance the response to tumor immunotherapy.

Automated summary

This study explores the potential clinical value and molecular mechanisms of miRNA-22 in tumor cell phagocytosis by macrophages and more efficient T cell priming. miR-22 upregulation enhances the phagocytic ability of macrophages, inhibits glioma cell proliferation and migration, and promotes antigen presentation and efficient T cell priming. The study also identifies HDAC6 as a target and NF-kappa B signaling as a pathway associated with miR-22 in tumor-associated macrophages of glioma.