Function of Insulin-like growth factor in neuroblastoma cell proliferation

Research Project

Project/Area Number	25461590
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Multi-year Fund
Section	一般
Research Field	Pediatrics
Research Institution	Mie University
Principal Investigator	Komada Yoshihiro 三重大学, 学内共同利用施設等, 学長 (80186791)
Co-Investigator(Kenkyū-buntansha)	Toyoda Hidemi 三重大学, 医学(系)研究科(研究院), 助教 (60525327)
Project Period (FY)	2013-04-01 – 2016-03-31
Project Status	Completed (Fiscal Year 2015)
Budget Amount *help	¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000) Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000) Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000) Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Keywords	神経芽腫 / インスリン様成長因子 / 細胞内増殖シグナル / インスリン様増殖因子 / 細胞増殖 / PDK1-mTOR経路 / AKT阻害剤 / mTOR阻害剤 / インスリン / アポトーシス細胞死 / オートクライン機構 / 細胞回転 / インスリン様増殖因子受容体 / インスリン受容体
Outline of Final Research Achievements	Insulin-like growth factor receptor (IGF-R) plays an important role on cancer cell proliferation. It has been shown that neuroblastoma (NB) cells can be categorized into three groups by the patterns of IGF-R pathway response. The IGF-R pathway can be activated by endogenous IGF in group 1 NB cells. Stimulation of IGF-R pathway can be induced by exogenous IGF in group 2 NB cells. Activated IGF-R pathway hardly accelerate the cell proliferation of group 3 NB cells. In addition, IGF-R growth stimulation can be mediated by several different intracellular signal transduction pathways. These results suggest that the significant heterogeneity of NB cells in IFG-R-mediated cell proliferation response should be taken enough into consideration, when any signal transduction inhibitors are used in the clinical treatment of NB patients.