Exosomal miRNA-7 from TWEAK-stimulated macrophages inhibiting the invasion and migration of ovarian cancer cells
Online published: 2017-07-05
Supported by
National Natural Science Foundation of China, 81272884; Foundation of Shanghai Municipal Commission of Health and Family Planning, ZHYYZXYJHZX-2-06; Shanghai Municipal Education Commission–Gaofeng Clinical Medicine Grant Support, 20161412
Objective · To determine the expression of miRNA-7 in TWEAK-stimulated macrophages and their secreted exosomes; to investigate the role of exosomal miRNA-7 from TWEAK-stimulated macrophages in modulating the metastasis of epithelial ovarian cancer (EOC) cells. Methods · Real-time PCR analysis was used to determine the miRNA-7 expression in TWEAK-stimulated macrophages, their exosomes and recipient HO8910-PM cells. The activity of EGFR signaling pathway in HO8910-PM cells was detected by Western blotting analysis. AntagomiR-7 was used to downregulate the miRNA-7 expressions in macrophage exosomes and then their effect on metastasis of HO8910-PM cells was examined by transwell assay. Results · TWEAK increased the levels of miRNA-7 in macrophages and their secreted exosomes and also resulted in an elevated level of miRNA-7 in recipient HO8910PM cells, which eventually reduced the activity of EGFR/AKT/ERK1/2 pathway. Pre-transfection of antagomiR-7 remarkably decreased the levels of miRNA-7 in macrophages, their secreted exosomes and the recipient EOC cells, with the enhancement of HO8910-PM metastasis. Conclusion · Exosomal miRNA-7 from TWEAK-stimulated macrophages plays a critical role in suppressing the metastasis of EOC cells by attenuation of EGFR signaling
pathway.
Key words: epithelial ovarian cancer; macrophages; exosome; TWEAK; cell invasion and migration
LI Dong , HU Yuan , WU An-yue , QIU Xing-di , QIU Li-hua . Exosomal miRNA-7 from TWEAK-stimulated macrophages inhibiting the invasion and migration of ovarian cancer cells[J]. Journal of Shanghai Jiao Tong University (Medical Science), 2017 , 37(6) : 726 . DOI: 10.3969/j.issn.1674-8115.2017.06.003
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