Abstract
Background: As a subtype of human genitourinary system cancer, the morbidity of bladder cancer (BC) continues to rise. Because of the high potentiality of cell metastasis, the 5-year survival rate of BC is relatively low. Long noncoding RNAs (lncRNAs) have been verified by a large body of literature to engage in the tumorigenesis of a few cancers. DDX11-AS1 has been elucidated as a malignancy promoter in several cancers; therefore, its mysterious role in BC attracted our interest as being well worth investigating. Aim of the Study: The primary consideration of this article was to clarify the part that DDX11-AS1 plays in the progression of BC. Methods: The expression of DDX11-AS1 in BC was revealed by quantitative real-time polymerase chain reaction. The biological functions of DDX11-AS1 in BC were evaluated through CCK-8 (Cell Counting Kit-8), EDU, TUNEL (TdT-mediated dUTP nick-end labeling), flow cytometry analysis, and Western Blot assays. Luciferase or RNA immunoprecipitation assay was used to investigate the interaction between miR-2355-5p and DDX11-AS1 (or LAMB3). Results: DDX11-AS1 manifested remarkably high level in BC and promoted the malignancy of BC. Moreover, miR-2355-5p was validated to be able to bind with DDX11-AS1 and inhibit cell proliferation in BC. Furthermore, our data suggested that LAMB3 expression was evidently upregulated in BC cells and inversely modulated by miR-2355-5p. Besides, LAMB3 may bind with miR-2355-5p. Ultimately, rescue assays indicated that the restrained development of BC in sh-DDX11-AS1#1-transfected cells could be restored by enforced expression of LAMB3. Conclusion: DDX11-AS1 facilitates the tumorigenesis of BC by the miR-2355-5p/LAMB3 axis.
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