The effect of Nitric Oxide (NO) treatment on renal cell cancer

2014 Fiscal Year Final Research Report

• Project/Area Number: 24592404
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Urology
• Research Institution: Kyoto Prefectural University of Medicine
• Principal Investigator: HONGO Fumiya 京都府立医科大学, 医学(系)研究科(研究院), 助教 (80291798)
• Co-Investigator(Kenkyū-buntansha): MIKI Tsuneharu 京都府立医科大学, 医学研究科, 教授 (10243239) ; KAWAUCHI Akihiro 滋賀医科大学, 医学部, 教授 (90240952) ; NAKAMURA Terukazu 京都府立医科大学, 医学研究科, 講師 (10381964) ; KIMURA Yasunori 京都府立医科大学, 医学研究科, 助教
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 腎癌 / 一酸化窒素 / sニトロソ化

Outline of Final Research Achievements

Purpose and methods: Nitric oxide (NO) is a signaling molecule. This post- translational modification by NO is known as S-nitrosylation. We examined the effect of the NO donor DETA-NONOate on the renal cell cancer cell lines; CAKI-1, NC65, and ACHN. Anti-S-nitroso-Cysteine antibody was applied as a primary antibody for immunohistochemistry. The biotin-switch technique was applied to detect specific S-nitrosylated proteins.
Results and conclusions: Significant up-regulation of S-nitrosylated proteins employed with NO donor was observed by immunohistochemistry. Specific S-nitrosylated proteins in ACHN cells were detected by the biotin-switch technique and included HSP90 (heat shock protein 90), GRP78 (HSP70 family), HSP70, and pyruvate kinase M2. In ACNH cells, Significant up regulation of S-nitrosylated HSP90 by western blot. Conclusions: Our data showed that NO treatment significantly increased S-nitrosylation of several proteins.

Free Research Field

泌尿器腫瘍学