MiR-600 mediates EZH2/RUNX3 signal axis to modulate breast cancer cell viability and sorafenib sensitivity.

Abstract

Breast cancer (BC) ranks as the most prevalent gynecologic tumor globally. Abnormal expression of miRNAs is concerned with the development of cancers such as BC. However, little is known about the role of miR-600 in BC. This work aimed to explore the role of miR-600 in the malignant progression and sorafenib sensitivity of BC cells. Expression and interaction of miR-600/EZH2/RUNX3 were analyzed by bioinformatics. qRT-PCR was utilized to assay RNA expression of miR-600 and mRNA expression of EZH2/RUNX3. The binding relationship between miR-600 and EZH2 was tested by dual luciferase assay and RNA immunoprecipitation (RIP). The effects of miR-600/EZH2/RUNX3 axis on the malignant behavior and sorafenib sensitivity of BC cells were detected by CCK-8 and colony formation assay. Low expression of miR-600 and RUNX3 in BC was found by bioinformatics and molecular assays. High expression of EZH2 in BC was negatively correlated with RUVX3. Dual luciferase assay and RIP demonstrated that MiR-600 could bind to EZH2. Cell assays displayed that miR-600 knockdown could foster the malignant progression of BC cells and reduce the sensitivity of BC cells to sorafenib. EZH2 knockdown or RUNX3 overexpression could offset the effect of miR-600 inhibitor on the malignant behavior and sorafenib sensitivity of BC cells. MiR-600 can hinder the malignant behavior of BC cells and foster sensitivity of BC cells to sorafenib via EZH2/RUNX3 axis, exhibiting themiR-600/EZH2/RUNX3 axis as a feasible therapeutic target for BC patients.