The mechanism of metastasis and metastasis suppression in gastric carcinoma by molecular interactions between intracellular target molecules and metastasis suppressor protein Nm23-H1

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K08951
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Gastroenterology
• Research Institution: Kochi Gakuen College (2016-2017); Kochi University (2015)
• Principal Investigator: MURAKAMI MASANAO 高知学園短期大学, その他部局等, 准教授(移行) (80571017)
• Co-Investigator(Kenkyū-buntansha): 大畑 雅典 高知大学, 教育研究部医療学系基礎医学部門, 教授 (50263976)
• Research Collaborator: Derek Kennedy グリフィス大学, エスキティス研究所, 准教授
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 胃がん / がん転移抑制 / Nm23-H1 / Asef / G3BP

Outline of Final Research Achievements

We had identified several molecules as a target protein of metastasis suppressor protein Nm23-H1. To clear the mechanism of how cancer cells were obtained ability of migration, we investigated the relationship between Nm23-H1 and candidate of binding proteins which we identified previously. ①Asef2 was identified as a target protein of Nm23-H1, which was stimulated by adenomatous polyposis coli. The GEF activity of Asef was enhanced in scirrhous type gastric carcinoma cell lines and then led to high migration activities, however exogenous Nm23-H1 again suppressed GEF activity. ②G3BP1, 2a and 2b (G3BPs) that are associated with breast cancer and pancreatic cancer, were also bound to Nm23-H1, but there was a difference in the binding strength. Each G3BP molecules have different functions. G3BP1 is known to associate with stress granules formation. Co-transfected cells of G3BPs and Nm23-H1 showed co-localization in the cytoplasm as punctate signals and in all cases.

Free Research Field

腫瘍ウイルス学