LncRNA CALML3-AS1 promotes tumorigenesis of bladder cancer via regulating ZBTB2 by suppression of microRNA-4316.

An increasing number of studies have elucidated the essential roles of long noncoding RNAs (lncRNAs) in tumor development. LncRNAs are also closely associated with bladder cancer (BCa) progression. In the present study, we screened out a novel lncRNA CALML3-AS1 with increased expression value in BCa tissues. Particularly, we showed that CALML3-AS1 overexpression correlates with advanced staging and an unsatisfactory prognosis. Functional experiments illustrated that CALML3-AS1 knockdown suppressed BCa cell proliferation, arrested cell-cycle progression and impaired migration and invasion while promoting apoptosis. Mechanistic investigation revealed that CALML3-AS1 directly interacts with miR-4316 and inhibits its availability in BCa cells, leading to elevated expression of ZBTB2. Consequently, ZBTB2 promotes BCa tumorigenesis through repressing p21 and facilitating PDK4 transcription. In conclusion, our findings demonstrate a novel CALML3-AS1-mediated process involved in BCa progression and indicate it might be a promising therapeutic target.

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