Project/Area Number |
26430152
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Tumor diagnostics
|
Research Institution | Osaka University (2016) National Institutes of Biomedical Innovation, Health and Nutrition (2014-2015) |
Principal Investigator |
Hara Yasuhiro 大阪大学, 医学系研究科, 特任研究員(常勤) (70568617)
|
Co-Investigator(Kenkyū-buntansha) |
久米 秀明 国立研究開発法人医薬基盤・健康・栄養研究所, 医薬基盤研究所 プロテオームリサーチプロジェクト, 協力研究員 (50322714)
足立 淳 国立研究開発法人医薬基盤・健康・栄養研究所, 医薬基盤研究所 プロテオームリサーチプロジェクト, サブプロジェクトリーダー (20437255)
朝長 毅 国立研究開発法人医薬基盤・健康・栄養研究所, 医薬基盤研究所 プロテオームリサーチプロジェクト, プロジェクトリーダー (80227644)
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | 大腸癌 / 膜タンパク質 / バイオマーカー |
Outline of Final Research Achievements |
We previously reported the identification of a number of membrane proteins which were increased in colorectal cancer tissues. These proteins appeared to be biomarker candidates for colorectal cancer. In this study, to investigate the relevance of these proteins to cancer progression, we performed screening for functions of these proteins against growth, migration, and invasion of colon cancer cells using siRNA knock-down. Consequently, we found two proteins that were significantly suppressed viability of cancer cells. SIGMAR1 is known to participate in ER stress regulation. Treatment of colon cancer cells with a SIGMAR1 agonist mitigated tunicamycin-induced ER stress. We assumed that SIGMAR1 facilitated cancer progression via suppression of ER stress. GGT5 is an enzyme metabolizing glutathione. Knock-down of GGT5 significantly reduced growth of colon cancer cells but not normal cells. Thus, GGT5 is likely to contribute the exploitation of therapeutic methods of colorectal cancer.
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