Dong Chen1, Junyi Chen1, Jialin Gao2, Yongrui Zhang2, Yongzhi Ma2, Wei Wei2, Yong Wei3. 1. Department of Urology, 2nd Affiliated Hospital of Fujian Medical University, Quanzhou City, China. 2. Urology, the First Hospital of Jilin University, Changchun City, China. 3. Department of Urology, Nanjing Gaochun People's Hospital, Nanjing, China.
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.
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.