Study on radiation induced bystander signaling between targeted human lung cancer cells and neighboring normal cells.

2015 Fiscal Year Final Research Report

• Project/Area Number: 25861137
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Radiation science
• Research Institution: National Institute of Radiological Sciences
• Principal Investigator: Konishi Teruaki 国立研究開発法人放射線医学総合研究所, 研究基盤センター, 研究員 (70443067)
• Research Collaborator: KOBAYASHI Alisa ; MAEDA Takeshi ; OIKAWA Masakazu ; FURUSAWA Yoshiya ; YU Peter ; DESAI Sejal ; PANDEY Badri
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: バイスタンダー効果 / マイクロビーム / ＤＮＡ二本鎖切断 / 窒素酸化物ラジカル / 細胞間情報伝達 / ギャップジャンクシャン / γＨ２ＡＸ

Outline of Final Research Achievements

Radiation cancer therapy is now one of the most successful method due technological innovations of the highly accurate and selective localization of the dose. The purpose of this study was to construct a simple model in radiotherapy, and to clarify the effect and its mechanism of cellular communication between irradiated cancer cells and non-irradiated normal cells. We applied microbeam irradiation technologies to target only the A549 human lung carcinoma cells in the mixed population of cells with human normal lung fibroblast cells. SPICE-NIRS microbeam was used to irradiate 500 protons of 3.4 MeV (LET: 12 Kiev/um in water) two nuclei of A549 cells. As a result, we found that two major pathways of radiation induced bystander response, media transfer signaling pathway and gap junction mediated signaling pathway mediate DNA double strand breaks repair pathway in irradiated A549 cells by non-irradiated WI-38 cells.

Free Research Field

放射線生物学