Exosomal miR-17-5p promotes angiogenesis in nasopharyngeal carcinoma via targeting BAMBI
Objective: The purpose of our study is to investigate the role of miR-17-5p in angiogenesis of nasopharyngeal carcinoma and the crosstalk between HUVECs and CNE-2 via exosomes. Methods: Firstly, flow cytometry, cell viability assay, transwell assay, and tube formation were used to explore the role o...
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Veröffentlicht in: | Journal of Cancer 2019-01, Vol.10 (26), p.6681-6692 |
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Sprache: | eng |
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Zusammenfassung: | Objective: The purpose of our study is to investigate the role of miR-17-5p in angiogenesis of nasopharyngeal carcinoma and the crosstalk between HUVECs and CNE-2 via exosomes. Methods: Firstly, flow cytometry, cell viability assay, transwell assay, and tube formation were used to explore the role of miR-17-5p in angiogenesis. Then zebrafish model was used to confirm effects of miR-17-5p on angiogenesis. qRT-PCR analysis and Immunofluorescence assay were used to explore the expression of miR-17-5p in NPC tissues and cells compared to the normal control. Besides, in vitro assays were used to analyze the biological functions of miR-17-5p in NPC. What's more, in vitro and in vivo assays were used to detect the function of exosomal miR-17-5p in angiogenesis. Finally, luciferase reporter assay and western bolt were used to determine the relationship between miR-17-5p and BAMBI. Results: We observed that high expression of miR-17-5p promoted angiogenesis in NPC. Also, high expression of miR-17-5p promoted the NPC cells proliferation and migration. To know whether there's any communication between HUVECs and NPC cells, exosomes derived from CNE-2 cells were collected. Further results showed that exosomal miR-17-5p secreted from NPC promoted the angiogenesis. What's more, in vitro assays revealed that miR-17-5p targets BAMBI and regulates AKT/VEGF-A signaling. Conclusions: Our study showed that exosomal miR-17-5p derived from NPC cells promotes angiogenesis via targeting BAMBI and regulates AKT/VEGF-A signaling. |
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ISSN: | 1837-9664 1837-9664 |
DOI: | 10.7150/jca.30757 |