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Elucidation of novel carcinogenesis / development pathway of bladder cancer by using metabolism-related omics analysis

Research Project

Project/Area Number 26462410
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Urology
Research InstitutionKyoto University

Principal Investigator

Terada Naoki  京都大学, 医学研究科, 助教 (60636637)

Co-Investigator(Kenkyū-buntansha) 松井 喜之  京都大学, 医学研究科, 助教 (00582107)
小林 恭  京都大学, 医学研究科, 特定病院助教 (00642406)
Project Period (FY) 2014-04-01 – 2017-03-31
Project Status Completed (Fiscal Year 2016)
Budget Amount *help
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Keywords膀胱癌 / 細胞老化
Outline of Final Research Achievements

It was confirmed that expression of PGAM1 was elevated in the order of normal urothelial cell line, noninvasive bladder cancer cell line, invasive bladder cancer cell line. In addition, analysis by public databases also confirmed an increase in expression of PGAM1 in bladder cancer specimens. However, in the analysis of tissue micriarrays of human clinical specimens, there was no correlation between the degree of invasion and the staining level of PGAM1.
Subsequently, when expression of PGAM1 was suppressed using shRNA, no change was observed in invasive and migratory ability, but the proliferative ability was decreased. In addition, when BBN was administered to wild type and PGAM 1 transgenic mice for 10 weeks, the PGAM 1 transgenic mouse group had a significantly higher carcinogenic rate.

Report

(4 results)
  • 2016 Annual Research Report   Final Research Report ( PDF )
  • 2015 Research-status Report
  • 2014 Research-status Report

URL: 

Published: 2014-04-04   Modified: 2018-03-22  

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