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Downregulation of CIP2A inhibits cancer cell proliferation and vascularization in renal clear cell carcinoma.

Authors
  • Gao, Hui1
  • Li, Yuqiao1
  • Lin, Tao1
  • Cheng, Yan1
  • Ma, Yunbo1
  • 1 Department of Urology, Liaocheng People's Hospital, Liaocheng City, Shandong Province, P. R. China, 252000. , (China)
Type
Published Article
Journal
Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia
Publication Date
Jun 01, 2020
Volume
164
Issue
2
Pages
196–202
Identifiers
DOI: 10.5507/bp.2019.031
PMID: 31431792
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

CIP2A has been proved to play a role as an oncogene in various types of malignancies while its functionality in renal clear cell carcinoma has not been investigated. Our study aimed to investigate the role of CIP2A in renal clear cell carcinoma and to explore the possible mechanisms. A total of 80 patients with renal clear cell carcinoma and 32 healthy people were included in the study. Expression of CIP2A was detected by qRT-PCR. CIP2A silencing renal clear cell carcinoma cell line was established. Its effects on cell proliferation and migration were verified by CCK-8 assay and Transwell cell assay, respectively. The effects of CIP2A overexpression on AKT and VEGF were investigated. CIP2A expression level was increased in tumor tissues compared to adjacent healthy tissues. Serum levels of CIP2A protein were higher in cancer patients than in healthy controls, and serum levels of CIP2A protein were increased with increased stage of primary tumor. Serum CIP2A protein can be used to accurately predict renal clear cell carcinoma and its prognosis. CIP2A siRNA silencing inhibited tumor cell proliferation, and treatment with Akt activator reduced this inhibitory effect. CIP2A siRNA silencing decreased the expression level of VEGF and phosphorylation levels of AKT in renal clear cell carcinoma cells, while AKT activator treatment showed no significant effects on CIP2A expression. Downregulation of CIP2A can inhibit cancer cell proliferation and vascularization in renal clear cell carcinoma through inactivation of the Akt pathway and its downstream VEGF.

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