MiR-9-5p could promote angiogenesis and radiosensitivity in cervical cancer by targeting SOCS5.

Abstract

The aim of this study was to investigate the molecular mechanism of miRNA-9-5p in cervical cancer. The expression level of microRNA-9-5p (miR-9-5p) in cervical cancer (CC) tissues and cell lines was examined by quantitative Real Time-Polymerase Chain Reaction. Cells were transfected with Lipofectamine 3000. Cell proliferation was measured by Cell Counting Kit-8 (CCK-8). Invasion assays were performed in 24-well transwell chambers system with 8 μm pores. Cell invasion was evaluated by transwell assay. Western blot was used to detect the changes of epithelial-mesenchymal transition (EMT) and SOCS5. The effects of miR-9-5p on tubule formation were examined under different doses of γ radiation. Immunohistochemistry assay was used to analyze the protein expression of SOCS5. Fluorescence microscopy analysis was used to measure autophagosomes after cells treated with γ irradiation. From the Cancer Genome Atlas (TCGA) database, the expression of miR-9-5p was significantly higher in cervical cancer patients than in the negative ones, and it was verified in 22 paired of lymph node-positive patient tissues and negative. The overexpression of miR-9-5p promoted proliferation and invasion of cervical cancer cells in vitro and primary tumor growth in vivo. MiR-9-5p reduced the tubule generation after the radiation dose of 4Gy. Besides, we identified SOCS5 as the target of miR-9-5p, and the overexpression of SOCS5 could inhibit miR-9-5p mimics from promoting tubule formation. MiR-9-5p could promote proliferation and invasion of CC cells in vitro and in vivo. MiR-9-5p could affect angiogenesis and radiosensitivity of CC cells by targeting SOCS5.