期刊
ONCOTARGET
卷 7, 期 28, 页码 43076-43087出版社
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.9246
关键词
exosomes; MiR-222-3p; macrophage; polarization; epithelial ovarian cancer
资金
- National Natural Science Foundation of China [81372787]
- Shanghai Municipal Bureau of Health [20134033]
- Shanghai Health System joint research project [2013ZYJB0201]
- Top 100 Medical Elite in Shanghai [XBR 2011065]
Cancer secreted exosomal miRNAs are emerging as mediators between tumor-stoma crosstalk. Here, we show epithelial ovarian cancer (EOC)-derived exosomes activated macrophages to a tumor-associated macrophage (TAM)-like phenotype with SOCS3/STAT3 pathway involvement, which could facilitate the progression of cancer. MiR-222-3p was enrichment in exosomes released from EOC cells and it could be transferred to macrophages. Overexpression of miR-222-3p in macrophages induced polarization of the M2 phenotype. Luciferase assay verified miR-222-3p targeted SOCS3 genes and expression of SOCS3 was decreased after transfection with a miR-222-3p mimic. Down-regulation of SOCS3 correlated with an increased expression of STAT3 activation. MiR-222-3p could be detected in the exosomes from serum and its levels were related to EOC. These observations propose tumor-derived exosomal miR-222-3p is an effective regulator in the polarization of tumor-promoting M2 macrophages and may be a biomarker of EOC.
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