Searching for new types of anti-cancer agents which modulate glucose transporter expression

2014 Fiscal Year Final Research Report

• Project/Area Number: 25640092
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Tumor therapeutics
• Research Institution: Iwate Medical University
• Principal Investigator: KITAGAWA Takayuki 岩手医科大学, 薬学部, 教授 (80092188)
• Co-Investigator(Kenkyū-buntansha): SAKYO Tomoko 岩手医科大学, 薬学部・細胞病態生物学講座, 助教 (00405755)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: 腫瘍生物学 / がん化学療法 / 分子標的治療薬 / 糖輸送タンパク質 / 糖代謝 / 膜たんぱく質

Outline of Final Research Achievements

Increased glucose uptake is fundamental to many solid tumors and well associated with increases in glycolysis and the over-expression of glucose transporters (GLUT) at the plasma membrane. Tumor-suppressed HeLa hybrid cells express GLUT1 alone, whereas the tumorigenic HeLa cell hybrids express GLUT1 and GLUT3, which were shown to be differential distribution within the plasma membranes. In previous studies, we identified GSK-3 inhibitors that selectively kill GLUT3-expressing tumorigenic HeLa cell hybrids by using a cell-based screening of compounds in chemical libraries (Oncogenesis 2012). In this study, we found inhibition of cell growth and GLUT3-expression by GSK-3 inhibitor was also evident in human colon cancers. In addition, GSK-3 inhibitor showed a partial inhibitory effect on the in vivo tumor growth of CGL4 cells. These results suggest a potential use of GSK-3 inhibitors to selectively kill cancer cells that modulate GLUT3-dependent glucose metabolism.

Free Research Field

腫瘍生物学