[No authors listed]
MiRNA (miR)-128, which is a wellârecognized inhibitor of tumor growth, is involved in the anti-tumor function of dendritic cells (DCs). However, the association between miRâ128 and the DCâmediated antiâtumor immunity remains to be elucidated. Murine B16 melanoma cells and C57BL/6 male mice were used to obtain marrowâderived DCs. DCs were treated with B16 cell suspension. miRâ128 mimic, miRâ128 inhibitor, p38 inhibitor or negative control oligonucleotides were transfected into DCs. After transfection, mRNA and protein expression of p38 in DCs was detected via reverse transcriptionâquantitative polymerase chain reaction and western blotting. The present study demonstrated that the miRâ128 abundance in DCs was significantly attenuated by B16 (a melanoma cell line) stimulation and the protein expression level of p38 was increased. Additionally, miRâ128 inhibited the protein expression of p38 in DCs in a doseâdependent manner, however no significant effect on the p38 mRNA level was observed. Furthermore, miRâ128 mimic or p38 inhibitor decreased the mRNA expression and secretion of interleukin (IL)â6 and ILâ10 cytokines and increased the level of ILâ12 in DCs, whereas an miRâ128 inhibitor exhibited the opposite effects. These findings suggested that miRâ128 regulated the immune response of DCs via p38âdownstream cytokines. Furthermore, the tumor growth rate, size and weight were markedly decreased and the survival time prolonged, following injection of DCs harboring miRâ128 mimic or p38 inhibitor in C57BL/6 mice bearing B16 melanoma. The results therefore suggest that miRâ128 enhances the antiâtumor immunity response of DCs via targeting of the p38 mitogen activated protein kinase signaling pathway.
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