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| Inhibition of the migration and invasion of ovarian cancer SKOV3 cells of SOX4 by miR-363-3p as targeted regulating |
| The Cangzhou Centre Hospital, Hebei Province, 061000 |
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Abstract To investigate the effect of miR-363-3p targeted regulating SOX4 on the migration and invasion of ovarian cancer SKOV3 cell. Methods: RT-qPCR was used to detect the expression of miR-363-3p and SOX4 in normal ovarian IOSE80 cells and ovarian cancer SKOV3 cells. After MiR-363-3p mimics and mimics NC were transferred into SKOV3 cells, the Transwell experiment was used to explore the effect of miR-363-3p on migration and invasion of SKOV3 cells. The mRNA and protein expressions of SOX4, vimentin, and E-cadherin were detected by RT-qPCR and Western blot, respectively. The luciferase reporter assay was used to verify the targeting relationship between miR-363-3p and SOX4. Results: Compared with those of the women with normal ovarian cells, the miR-363-3p expression in SKOV3 cells of the women with ovarian cancer had decreased significantly, while the SOX4 expression had increased significantly (P＜0.05). The over expression of miR-363-3p in SKOV3 cells could inhibit the migration and invasion of SKOV3 cells (P＜0.05). RT-qPCR and Western blot results showed that the expressions of SOX4 and vimentin of the cell with miR-363-3p positive mimics transferring were significant lower than those of the cell with miR-3633p negative of mimics and those of the cell in blank control group, while the expression of E-cadherin of the cell with miR-363-3p positive mimics transferring were significant higher than those of the cell with miR-363-3p negative of mimics and those of the cell in blank control group was significantly higher than that of mimics NC group and blank control group (P＜0.05). MiR-363-3p could targeted regulating the expression of SOX4 of 3'-UTR (P＜0.05). Conclusion: miR-3633p promotes SOX4 degradation by binding to the 3'-UTR of SOX4 mRNA, thereby it can inhibiter the migration and invasion of ovarian cancer cells by downregulating vimentin level and up-regulating the activity of E-cadherin.
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