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Your search keyword '"Yang, Chengdi"' showing total 2 results
Start Over Author "Yang, Chengdi" Publisher cell physiol biochem press gmbh & co kg
2 results on '"Yang, Chengdi"'

1. CircRNA-Cdr1as Exerts Anti-Oncogenic Functions in Bladder Cancer by Sponging MicroRNA-135a.

Author

Li P, Yang X, Yuan W, Yang C, Zhang X, Han J, Wang J, Deng X, Yang H, Li P, Tao J, Lu Q, and Gu M

Subjects
Animals, Antagomirs metabolism, Cell Line, Tumor, Cell Movement, Cell Proliferation, Female, Humans, In Situ Hybridization, Fluorescence, Mice, Mice, Inbred BALB C, Mice, Nude, MicroRNAs antagonists & inhibitors, MicroRNAs genetics, RNA, Long Noncoding genetics, Transplantation, Heterologous, Urinary Bladder Neoplasms genetics, Urinary Bladder Neoplasms metabolism, MicroRNAs metabolism, RNA, Long Noncoding metabolism, Urinary Bladder Neoplasms pathology
Abstract

Background/aims: CircRNAs regulate gene expression in different malignancies. However, the role of Cdr1as in the tumourigenesis of bladder cancer and its potential mechanisms remain unknown., Methods: qRT-PCR was used to detect Cdr1as and target miRNA expression in bladder cancer tissues and cell lines. Biological functional experiments were performed to detect the effects of Cdr1as on the biological behaviour of bladder cancer cells in vivo and in vitro. Bioinformatic analysis was utilised to predict potential miRNA target sites on Cdr1as. Ago2 RNA binding protein immunoprecipitation assay, RNA antisense purification assay, biotin pull down assay and RNA FISH were performed to detect the interaction between Cdr1as and target miRNAs. Western blot was used to determine the expression level of p21 in bladder cancer cells., Results: Cdr1as was significantly down-regulated in bladder cancer tissues compared with adjacent normal tissues. Overexpression of Cdr1as inhibited the proliferation, invasion and migration of bladder cancer cells in vitro and slowed down tumour growth in vivo. Cdr1as sponged multiple miRNAs in bladder cancer. Moreover, Cdr1as directly bound to miR-135a and inhibited its activity in bladder cancer., Conclusion: Cdr1as is down-regulated and sponges multiple miRNAs in bladder cancer. It exerts anti-oncogenic functions by sponging microRNA-135a., (© 2018 The Author(s). Published by S. Karger AG, Basel.)

Published
2018
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2. MicroRNA-218 Increases the Sensitivity of Bladder Cancer to Cisplatin by Targeting Glut1.

Author

Li P, Yang X, Cheng Y, Zhang X, Yang C, Deng X, Li P, Tao J, Yang H, Wei J, Tang J, Yuan W, Lu Q, Xu X, and Gu M

Subjects
Base Sequence, Binding Sites, Cell Line, Tumor, Cell Survival drug effects, Epithelial Cells metabolism, Epithelial Cells pathology, Genes, Reporter, Glucose antagonists & inhibitors, Glucose metabolism, Glucose Transporter Type 1 antagonists & inhibitors, Glucose Transporter Type 1 metabolism, Glutathione agonists, Glutathione metabolism, Humans, Inhibitory Concentration 50, Luciferases genetics, Luciferases metabolism, MicroRNAs agonists, MicroRNAs metabolism, Signal Transduction, Urinary Bladder drug effects, Urinary Bladder metabolism, Urinary Bladder pathology, Antineoplastic Agents pharmacology, Cisplatin pharmacology, Epithelial Cells drug effects, Gene Expression Regulation, Neoplastic, Glucose Transporter Type 1 genetics, MicroRNAs genetics
Abstract

Background/aims: MicroRNA-218 (miR-218) is down-regulated in many malignancies that have been implicated in the regulation of diverse processes in cancer cells. However, the involvement of miR-218 in chemo-sensitivity to cisplatin and the precise mechanism of this action remained unknown in bladder cancer., Methods: qRT-PCR was used to detect miR-218 and its target Glut1 expression in bladder cancer cell lines T24 and EJ. CCK-8 method was utilized to measure the cell viability. IC 50 was calculated via a probit regression model. Glut1 was detected by western blotting for analysis of potential mechanism. Luciferase reporter assay was utilized to validate Glut1 as a direct target gene of miR-218. The intracellular level of GSH and ROS were determined using a commercial colorimetric assay kit and 2', 7'-dichlorodihydro-fluorescein diacetate, respectively., Results: Over-expression of miR-218 significantly reduced the rate of glucose uptake and total level of GSH and enhanced the chemo-sensitivity of bladder cancer to cisplatin. Mechanistically, Glut1 was found to be a direct and functional target of miR-218. Up-regulation of Glut1 could restore chemo-resistance in T24 and EJ cells. On the contrary, knockdown of Glut1 could generate a similar effect as up-regulating the expression of miR-218., Conclusions: MiR-218 increases the sensitivity of bladder cancer to cisplatin by targeting Glut1. Restoration of miR-218 and repression of glut1 may provide a potential strategy to restore chemo-sensitivity in bladder cancer., (© 2017 The Author(s)Published by S. Karger AG, Basel.)

Published
2017
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