Increased motility of cancer cells through surface trafficking of GluR1 AMPA receptors by nitric oxide in response to ionizing radiation

2014 Fiscal Year Final Research Report

• Project/Area Number: 23390352
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Neurosurgery
• Research Institution: University of the Ryukyus
• Principal Investigator: ISHIUCHI Shogo 琉球大学, 医学(系)研究科(研究院), 教授 (10312878)
• Co-Investigator(Kenkyū-buntansha): NAGAMINE Hideki 琉球大学, 大学院医学研究科, 助教 (30573331) ; TSUTSUI Masato 琉球大学, 大学院医学研究科, 教授 (70309962) ; WATANABE Takashi 琉球大学, 医学部附属病院, 講師 (90573337)
• Co-Investigator(Renkei-kenkyūsha): YOSHIDA Yukari 群馬大学, 重粒子線医学センター, 助教 (90431717) ; TSUZUKI Keisuke 文教大学, 健康栄養学部管理栄養学科, 教授 (60222139)
• Project Period (FY): 2011-04-01 – 2015-03-31
• Keywords: 神経膠芽腫 / 浸潤性増殖 / 放射線抵抗性 / 重粒子線 / 遊走阻害剤

Outline of Final Research Achievements

Cells response to various exogenous stimuli, and can propagate signals by several pathways. Here we show that nitric oxide ( NO ) is produced in response to ionizing radiation and fulfils a broad spectrum of signaling for pathophysiological process of invasive growth in brain cancers. NO mediates a stimulatory sign that leads to tumor cells outside irradiated field. High linear energy transfer charged particle (LET) as well as X-ray radiation stimulated NO production in cancer cells and the increased mobility through facilitation of surface trafficking of GluR1, a subunit of AMPA-type glutamate receptor (AMPAR), via cGMP-dependent signal transduction and activation of intracellular calcium signaling . Blockage of AMPAR by antagonists or knockdown of GluR1 reduced NO production and propagation, and can regulate this invasive growth.

Free Research Field

脳神経外科学