Elucidation of Arf6 signaling mechanism to generate novel anticancer drugs

Research Project

Project/Area Number	16K19014
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Multi-year Fund
Research Field	General pharmacology
Research Institution	University of Tsukuba
Principal Investigator	Katagiri Naohiro 筑波大学, 医学医療系, 助教 (70755686)
Research Collaborator	Fujii Ikuo 大阪府立大学, 大学院理学系研究科, 教授 Fujiwara Daisuke 大阪府立大学, 大学院理学系研究科, 助教
Project Period (FY)	2016-04-01 – 2018-03-31
Project Status	Completed (Fiscal Year 2017)
Budget Amount *help	¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000) Fiscal Year 2017: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000) Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Keywords	Arf6 / ARF6 / 抗がんペプチド / 低分子Gタンパク質 / 癌抑制ペプチド / シグナル伝達 / 薬理学 / 癌
Outline of Final Research Achievements	This study was carried out to generate peptides that specifically suppress the small molecule G protein ARF6 involved in tumor angiogenesis and cancer cell invasion / metastasis. First, peptides binding to ARF6 were screened by using the phage display assay. As a result of screening using a phage library expressing a peptide consisting of random 39 amino acids, 71 kinds of peptides that bind to ARF6 were identified. The ARF6 binding ability of the identified peptides were confirmed by ELISA. Furthermore, Arf6 inhibitory ability of the identified Arf6-binding peptide were evaluated by fluorescent nucleotide exchange assay. As a result of the experiments, several peptides showed Arf6 specific inhibitory ability.