Long noncoding RNA MAFG-AS1 facilitates bladder cancer tumorigenesis via regulation of miR-143-3p/SERPINE1 axis.

Abstract

BackgroundNumerous studies have shown that long noncoding RNAs (lncRNAs) act as key regulators of bladder cancer progression. While lncRNA MAFG-AS1 has been confirmed as an oncogenic molecule in various cancers and tumorigenesis, in present study, we investigated its function and role in the tumorigenesis of bladder cancer.MethodsThe expression of MAFG-AS1, miR-143-3p and SERPINE1 in bladder cancer tissues was detected by qRT-PCR methods. The relationship between MAFG-AS1 expression and clinicopathologic characteristics of bladder cancer was analyzed. The effects of MAFG-AS1 depletion on cell proliferation, migration, invasion and apoptosis were investigated. The binding relationship of MAFG-AS1, miR-143-3p and SERPINE1 was examined by luciferase reporter analysis and RNA immunoprecipitation (RIP) assay.ResultsMAFG-AS1 was upregulated in bladder cancer tissues and cell lines. High MAFG-AS1 expression was associated with bladder cancer histological grade, TNM stage and lymph node metastasis, and patients with high expression showed poor overall survival. Cell function experiments showed that MAFG-AS1 silencing markedly suppressed bladder cancer cell proliferation, migration, invasion and increased cell apoptosis. Moreover, our results demonstrated that MAFG-AS1 functioned as a competing endogenous RNA for miR-143-3p to modulate SERPINE1 levels. Further analysis showed that miR-143-3p inhibition or SERPINE1 overexpression alleviated the suppressive effects of MAFG-AS1 silencing on malignant features.ConclusionsOur findings indicated that MAFG-AS1 facilitates tumorigenesis via regulation of the miR-143-3p/SERPINE1 axis and also provides a novel insight into tumorigenesis and identify a promising therapeutic target for bladder cancer.