Circ_0000511 accelerates the proliferation, migration and invasion, and restrains the apoptosis of breast cancer cells through the miR‑326/TAZ axis.

Abstract

Circular RNA 0000511 (circ_0000511) has been observed to be dysregulated in breast cancer (BC). However, the functions of circ_0000511 in breast cancer remain unknown. The expression levels of circ_0000511, ribonuclease P RNA component H1, microRNA-326 (miR-326) and transcriptional co-activator with PDZ-binding motif (TAZ) were examined by reverse transcription-quantitative PCR. Colony formation and MTT assays were conducted to analyze the cellular proliferative ability. The apoptotic rate was assessed by flow cytometry. Western blot analysis was used to evaluate the expression levels of B cell leukemia/lymphoma 2 (Bcl-2), Bcl-2 associated X apoptosis regulator, cleaved caspase-3 and TAZ. Transwell assays were performed to evaluate the migration and invasion of BC cells. The target interaction between miR-326 and circ_0000511 or TAZ was confirmed by dual-luciferase reporter assay. Xenograft assay was used to identify the function of circ_0000511 in vivo. Circ_0000511 abundance was abnormally elevated in BC tissue samples and cell lines compared with in matched normal cases. Circ_0000511 interference suppressed the proliferation, migration and invasion, and induced apoptosis of BC cells. miR-326 was a direct target of circ_0000511, and circ_0000511 silencing-mediated effects in BC cells were largely reversed by the knockdown of miR-326. miR-326 directly bound to TAZ mRNA, and TAZ accumulation largely attenuated miR-326 overexpression-induced effects in BC cells. Circ_0000511 upregulated the expression levels of TAZ partly via targeting miR-326 in BC cells. Circ_0000511 silencing restrained tumor growth in vivo. Circ_0000511 accelerated the proliferation, migration and invasion, while inhibiting the apoptosis of BC cells through upregulating TAZ expression via sponging miR-326. The circ_0000511/miR-326/TAZ axis may be a novel therapeutic target for BC treatment.