Long noncoding RNA EZR-AS1 promotes tumor growth and metastasis by modulating Wnt/β-catenin pathway in breast cancer.

Abstract

Accumulating evidence has demonstrated that long noncoding RNAs (lncRNAs) serve important roles in tumor development and progression. However, whether lncRNA EZR-AS1 is associated with breast cancer (BC) progression remains unclear. In the present study, reverse transcription-quantitative polymerase chain reaction analysis demonstrated that the expression of EZR-AS1 was significantly upregulated in BC tissues and cell lines. Furthermore, Kaplan-Meier curve analysis revealed that increased EZR-AS1 expression in patients with BC contributes to poor prognosis. Cell counting kit-8 and fluorescence-activated cell sorting experiments indicated that EZR-AS1 knockdown significantly suppressed the proliferation and cell cycle progression of breast cancer cells, while reducing cellular apoptosis. Furthermore, Transwell assays suggested that EZR-AS1 knockdown reduced the migration and invasion ability of BC cells compared with control cells. In the present study, it was observed that EZR-AS1 interacts with β-catenin to prevent degradation. EZR-AS1 knockdown resulted in β-catenin downregulation and inactivation of the Wnt/β-catenin pathway. Rescue assays revealed that β-catenin overexpression reversed the effects of EZR-AS1 knockdown on BC cell proliferation, apoptosis, migration and invasion. In conclusion, the results of the present study demonstrate that EZR-AS1 serves as an oncogene in BC via activating the Wnt/β-catenin pathway. This suggests that EZR-AS1 may be a therapeutic target for BC treatment.