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The Anti-tumor Role And Mechanism Of MiR-502-5p In Bladder Cancer

Posted on:2021-05-31Degree:MasterType:Thesis
Country:ChinaCandidate:Y F YingFull Text:PDF
GTID:2404330614968383Subject:Surgery
Abstract/Summary:PDF Full Text Request
Emerging evidence has shown that bladder cancer becomes more and more common in the world and rank the second in tumors of urinary system;New therapies came out every year to control it but its progress and metastasis still threaten the patients.While various therapeutic strategies have been proposed and used in past decades,radical cystectomy is considered the standard treatment for nonmetastatic MIBC.Patients with invasive BCa have a low 5-yr survival(62%)after radical cystectomy.Continuing efforts to create novel and more effective treatments are needed.Micro RNA are small non-coding RNAs that showed potential to be target gene regulators in the therapy of tumors recently,and many mi RNAs were proved to be involved in bladder cancer proliferation and migration.The main investigations and results are as follows:1)RT-q PCR was performed to examine the expression of mi R-502-5p in bladder cancer.Mi R-502-5p is frequently downregulated in BCa.Meanwhile,hypermethylation of Cp G islands contributes to the down-regulation of mi R-502-5p.2)Then transwell assay,colony formation assay,CCK8 assay,and flow cytometry analysis were applied to evaluate the function of mi R-502-5p in bladder cancer cell lines.Western blot was conducted to measure the protein levels of related genes.3)Furthermore,dual-luciferase reporter assay,in vivo tumorigenesis assay and immunohistochemical staining were also conducted as needed.In conclusion,we proved that overexpression of mi R-502-5p suppressed the proliferation and EMT progression by regulating its direct targets CCND1,DNMT3 B and NOP14 in bladder cancer,which may contribute to the development of new therapies against bladder cancer in the future.
Keywords/Search Tags:miR-502-5p, bladder cancer, epithelial–mesenchymal transition, CCND1, DNMT3B, NOP14
PDF Full Text Request
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