miR-66U-5p Targets TET2 to Promote Breast Cancer Proliferation,Migration and Invasion
Objective To study the mechanism of miR-660-5p/TET2 regulating the proliferation,apoptosis,migration and invasion of breast cancer cells through PI3K/AKT/mTOR signaling pathway.Methods The samples of breast cancer tissues and adjacent normal tissues of 65 patients with breast cancer in Jingmen People's Hospital from January 2021 to June 2022 were collected.The expression level of miR-660-5p in breast cancer tissues and cell lines was detected by qPCR.Kaplan-Meier survival analysis and log-rank test were used to analyze the correlation between miR-660-5p and clinicopathological features of patients.The effects of miR-660-5p on the proliferation,apoptosis,migration and invasion of breast cancer cells were detected by CCK8,flow cytometry and Transwell methods.The relationship between miR-660-5p and TET2 was determined by dual luciferase reporter gene and Western blotting.Western blot,CCK8 and Transwell experiments were used to confirm that miR-660-5p regulated breast cancer progression by targeting TET2.Whether miR-660-5p/TET2 activated PI3K/AKT/mTOR signal pathway was detected by Western blot experiment.The effect of knockdown of miR-660-5p in breast cancer was further proved through animal tumor formation experiment.Results The expression of miR-660-5p was up-regulated in breast cancer tissues,and the high expression of miR-660-5p was closely related to the lymph node metastasis(P=0.003),advanced TNM staging(P=0.009)and vascular invasion(P=0.018)of breast cancer.Knockdown of miR-660-5p inhibited breast cancer cell proliferation,migration and invasion,and induced breast cancer cell apoptosis.TET2 was the direct target of miR-660-5p,interference with TET2 could partially reverse the inhibitory effect of knockdown miR-660-5p on the malignant potential of breast cancer cells.miR-660-5p down-regulated TET2 and activated PI3K/AKT/mTOR signaling pathway.Knockdown of miR-660-5p inhibited tumor growth in vivo.Conclusions miR-660-5p promotes breast cancer progression by targeting TET2 and PI3K/AKT/mTOR signaling pathways,and may be a potential target for breast cancer treatment.
Breast cancermiR-660-5pTET2PI3K/AKT/mTOR signaling pathway