Background: Numerous 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.
Methods: The 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.
Results: MAFG-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.
Conclusions: Our 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.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8799265 | PMC |
http://dx.doi.org/10.21037/tcr-20-1971 | DOI Listing |
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