RESUMEN
@# Objective: To investigate the regulatory effect of miR-1297 on the malignant biological behaviors of breast cancer cells and its underlying mechanism. Methods: Twenty pairs of breast cancer tissues and para-cancer tissues resected at the Department of Thyroid and Breast Surgery of Leshan People′ s Hospital from May 2016 to May 2018, as well as breast cancer cell lines MCF-7, SW626, HCC1937 and human breast epithelial MCF-10A cells were collected for this study. qPCR was performed to evaluate the expression of miR-1297 in breast cancer tissues and cell lines. The experimental cells were divided into control group, miR-1297 inhibitor group; TET3 over-expression group and simultaneous over-expression of TET3 and miR-1297 group. CCK-8 assay was used to detect the cell proliferation of MCF-7 cells; Transwell assay was carried out to detect the migration and invasion of MCF-7 cells; and WB was used to measure the expressions of TET3 and EMT related proteins (E-cadherin, N-cadherin and vimentin). Dual luciferase reporter gene assay was used to verify the relationship between miR-1297 and TET3. Results: miR-1297 was up-regulated in both breast cancer tissues and cell lines (P<0.01 or P<0.05). Knockdown of miR-1297 dramatically repressed the proliferation, migration, invasion and EMT of MCF-7 cells (P<0.01 or P<0.05). Over-expression of TET3 significantly up-regulated the expression of TET3 in MCF-7 cells (P<0.05). Simultaneous over-expression of TET3 and miR-1297 could reverse the expression level of TET3 in MCF-7 cells and the inhibitory effect of TET3 on the proliferation, migration, invasion and EMT of MCF-7 cells. Dual luciferase reporter gene assay results showed that miR-1297 targetedly bound to the 3' UTR of TET3. Further experiment results demonstrated that miR-1297 targetedly down-regulated TET3 and promoted the malignant biological behaviors of MCF-7 cells. Conclusion: miR-1297 is up-regulated in breast cancer tissues and cells; it promotes the malignant biological behaviors such as proliferation, migration, invasion and EMT through targetedly down-regulating the expression of TET3.