| Co-Investigator(Kenkyū-buntansha) |
立井 一明 群馬大学, 医学(系)研究科(研究院), 准教授 (00192633)
大嶋 紀安 群馬大学, 医学(系)研究科(研究院), 助教 (30360514)
岸本 幸治 徳島大学, 生物資源産業学部, 講師 (50280699)
山本 正道 京都大学, 医学(系)研究科(研究院), 講師 (70423150)
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| Budget Amount *help |
¥18,590,000 (Direct Cost: ¥14,300,000、Indirect Cost: ¥4,290,000)
Fiscal Year 2015: ¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2014: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2013: ¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2012: ¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
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| Outline of Final Research Achievements |
G2A is a G protein-coupled receptor that uses oxidized free fatty acids as ligands. The addition of oxidized free fatty acids such as 9-HODE to the cultured cells resulted in cell cycle arrest. G2A induction was also observed by stress stimulation such as glucose starvation and hypoxia. It became clear that G2A induction is deeply involved in changes in intracellular pH and glutathione concentration. When glioma cells expressing G2A were transplanted into immunodeficient mice, tumor-formation and metastasis to the organs was observed. Immunohistochemical analysis of metastatic lesion revealed that epithelial mesenchymal transition occurred.
Thus, G2A, a stress-inducible GPCR, stops the cell cycle in response to oxidized free fatty acids. On the other hand, G2A increases stemness in tumor cells resulting in epithelial mesenchymal transition and forms metastatic foci.
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