MicroRNA-155 deficiency enhances the recruitment and functions of myeloid-derived suppressor cells in tumor microenvironment and promotes solid tumor growth.

摘要: Immune cells in tumor microenvironment play a prominent role progression and metastasis. MicroRNA-155 (miR-155) represents an important player innate adaptive immunity by regulating differentiation, maturation activation of macrophages, dendritic cells, B T cells. However, the miR-155 expression immune solid development is less elucidated. Our current study showed that both B16-F10 melanoma Lewis lung carcinoma (LLC) tumors grew much faster bic/miR-155 knockout (miR-155−/−) mice along with increase myeloid-derived suppressor (MDSCs) accumulation tumors, compared to wild-type mice. Bone marrow transplantation bone deficiency could replicate above tumor-promoting phenotype. In vitro demonstrated tumor-infiltrating miR-155−/− MDSCs greater migration ability expressed higher level multiple chemokines. Furthermore, we found HIF-1α, direct target miR-155, was increased deficient MDSCs, HIF-1α up-regulated CXCL1, CXCL3 CXCL8 contributing enhanced recruitment tumors. Moreover, immunosuppressive pro-angiogenic capacities. Taken together, our study, for first time, promoted growth through increasing enhancing functions recruited MDSCs. Thus, upregulating may be developed as therapeutic approach halt development.