BACKGROUND: MicroRNAs are a class of endogenous single strand non-coding RNAs that are involved in many important physiological and pathological processes. The purpose of this study was to investigate the expression levels of miR-29c in human bladder cancer and its potential role in disease pathogenesis. METHODS: The expression level of miR-29c was measured in 40 bladder cancer specimens and adjacent normal breast tissues by quantitative polymerase chain reaction (qPCR). Over-expression of miR-29c was established by transfecting mimics into T24.MTT assays, colony formation assays, transwell assays and cell cycle assays were used to explore the potential function of miR-29c inT24 bladder cancer cells. Luciferase reporter assays were performed to analyze the regulation of putative target of miR-29c. The effects of modulating miR-29c on endogenous levels of this target were subsequently confirmed via qRT-PCR and Western blot. RESULTS: The expression of miR-29c in bladder cancer specimens was lower than adjacent normal tissues (P<0.01). Overexpression of miR-29c inhibited cellular growth, suppressed cellular migration and caused an accumulation of cells in the G1 phase of the cell cycle, Dual-luciferase reporter assays showed that miR-29c binds the 3'-untranslated region (3'-UTR) of CDK6, suggesting that CDK6 is a direct target of miR-29c. Furthermore, through qPCR and Western blot assays confirmed that overexpression of miR-29c reduced CDK6 mRNA and protein levels. CONCLUSIONS: miR-29c could inhibit the proliferation, migration and invasion of bladder cancer cells via regulating CDK6. in the future, it could be used as a therapeutic target for the treatment of bladder cancer.
BACKGROUND: MicroRNAs are a class of endogenous single strand non-coding RNAs that are involved in many important physiological and pathological processes. The purpose of this study was to investigate the expression levels of miR-29c in humanbladder cancer and its potential role in disease pathogenesis. METHODS: The expression level of miR-29c was measured in 40 bladder cancer specimens and adjacent normal breast tissues by quantitative polymerase chain reaction (qPCR). Over-expression of miR-29c was established by transfecting mimics into T24.MTT assays, colony formation assays, transwell assays and cell cycle assays were used to explore the potential function of miR-29c inT24 bladder cancer cells. Luciferase reporter assays were performed to analyze the regulation of putative target of miR-29c. The effects of modulating miR-29c on endogenous levels of this target were subsequently confirmed via qRT-PCR and Western blot. RESULTS: The expression of miR-29c in bladder cancer specimens was lower than adjacent normal tissues (P<0.01). Overexpression of miR-29c inhibited cellular growth, suppressed cellular migration and caused an accumulation of cells in the G1 phase of the cell cycle, Dual-luciferase reporter assays showed that miR-29c binds the 3'-untranslated region (3'-UTR) of CDK6, suggesting that CDK6 is a direct target of miR-29c. Furthermore, through qPCR and Western blot assays confirmed that overexpression of miR-29c reduced CDK6 mRNA and protein levels. CONCLUSIONS:miR-29c could inhibit the proliferation, migration and invasion of bladder cancer cells via regulating CDK6. in the future, it could be used as a therapeutic target for the treatment of bladder cancer.
Authors: M Chilosi; C Doglioni; Z Yan; M Lestani; F Menestrina; C Sorio; A Benedetti; F Vinante; G Pizzolo; G Inghirami Journal: Am J Pathol Date: 1998-01 Impact factor: 4.307
Authors: Ramiro Garzon; Shujun Liu; Muller Fabbri; Zhongfa Liu; Catherine E A Heaphy; Elisa Callegari; Sebastian Schwind; Jiuxia Pang; Jianhua Yu; Natarajan Muthusamy; Violaine Havelange; Stefano Volinia; William Blum; Laura J Rush; Danilo Perrotti; Michael Andreeff; Clara D Bloomfield; John C Byrd; Kenneth Chan; Lai-Chu Wu; Carlo M Croce; Guido Marcucci Journal: Blood Date: 2009-02-11 Impact factor: 22.113
Authors: Yong-Hao Nan; Jun Wang; Yao Wang; Peng-Hao Sun; Yu-Ping Han; Li Fan; Kai-Chen Wang; Fu-Jun Shen; Wei-Hua Wang Journal: Am J Transl Res Date: 2016-11-15 Impact factor: 4.060