The incidence and mortality rate of bladder cancer have dramatically expanded, so it's urgent to discover new biomarker and therapeutic target for bladder cancer. Recently, lncRNA has been identified as oncogene or tumor suppressor to regulate the tumorigenesis. LncRNA ZFAS1 has been confirmed as oncogene in various tumors. However, the expression, function, and underlying mechanism of ZFAS1 in bladder carcinogenesis have yet to be totally clarified. In the current study, our data demonstrated that ZFAS1 expression was significantly upregulated in bladder cancer tissues and cell lines. Furthermore, Kaplan-Meier analysis revealed that high ZFAS1 expression was significantly associated with unfavorable progression free survival (PFS) (P = 0.0034 < 0.01) and overall survival (OS) (P = 0.0041 < 0.01) of bladder cancer patients. Moreover, silencing of ZFAS1 expression could markedly suppress bladder cancer cells proliferation and colony formation, arrest cell cycle, promote cell apoptosis and inhibit cell migration in vitro. In addition, bioinformatics analysis, luciferase reporter assay, and pull down assay revealed that ZFAS1 straightly interacted with miR-329. Lastly, rescue experiments confirmed that miR-329 inhibitor reversed the tumor suppressing roles of ZFAS1 knockdown on bladder cancer cells. Collectively, our results illuminated that ZFAS1 could serve as an oncogene in the tumorigenesis of bladder cancer, and discovered the functional regulatory network of ZFAS1 sponging miR-329.
Keywords: Bladder cancer; Tumorigenesis; ZFAS1; miR-329.
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