Characterization of mitochondrial function and development of antitumor tools based on p14 MIS peptide
Project/Area Number |
15K08415
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Experimental pathology
|
Research Institution | Niigata University |
Principal Investigator |
Saito Ken 新潟大学, 医歯学系, 准教授 (70426584)
|
Co-Investigator(Kenkyū-buntansha) |
近藤 英作 新潟大学, 医歯学系, 教授 (30252951)
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
Keywords | ペプチド / 癌 / ミトコンドリア / 抗腫瘍効果 |
Outline of Final Research Achievements |
In the present study, we report the development of r9-CatB-p14MIS peptide which enhances the antitumor effects in many cancer cells. The r9-CatB-p14MIS peptide translocated effectively to the mitochondria and triggered a reduction of mitochondrial membrane potential compared with prototype p14ARF peptides. In addition, cancer cells exhibited different levels of sensitivity to r9-Cat B-p14MIS peptide and the antitumor effects by the peptide were dependent on the expression of endogenous mitochondrial p14ARF, ATPAF1 (F1-ATPase assembly protein) and the magnitude of mitochondrial membrane potential. Furthermore, delivery of r9-CatB-p14MIS to the xenografted pancreatic tumor in mice suppressed tumor volume and cellular proliferation. These results suggested that r9-CatB-p14MIS was useful as novel antitumor molecule.
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Report
(4 results)
Research Products
(8 results)