@misc{oai:repo.qst.go.jp:00066525,
 author = {Kobayashi, Alisa and Autsavapromporn, Narongchai and Ahbrizal, Farizal Tengku Ahmad Tengku and Oikawa, Masakazu and Homma-Takeda, Shino and Furusawa, Yoshiya and Wang, Jun and Konishi, Teruaki and 小林 亜利紗 and 及川 将一 and 武田 志乃 and 古澤 佳也 and 小西 輝昭},
 month = {Nov},
 note = {The mechanisms underlying bi-directional signaling involved in radiation-induced bystander effect (RIBE) between irradiated carcinoma cells and their surrounding non-irradiated normal cells is relevant to radiation cancer therapy. Using the SPICE-NIRS microbeam, we delivered 500 protons to A549-GFP lung carcinoma cells, stably expressing H2B-GFP, that were co-cultured with normal WI-38 cells. The level of γ-H2AX, a marker for DNA double-strand breaks (DSB), was subsequently measured up to 24 h post irradiation in both targeted and bystander cells. As a result, gap junction intercellular communication (GJIC) inhibition attenuated DSB repair in targeted A549-GFP cells, and RIBE was suppressed in bystander WI-38 cells but not in distant A549-GFP cells. This suggested that GJIC plays a two-way role either propagating DNA damage effect between carcinoma to normal cells, or reversing the bystander signaling, also called a “rescue effect” from bystander cells to irradiated cells, in order to enhance the DSB repair in targeted cells., MICROS 2017 17th International Symposium on Microdosimetry},
 title = {Bystander WI-38 normal lung fibroblast cells modulate DNA double-strand break repair in microbeam-targeted A549 cells through gap junction intercellular communication},
 year = {2017}
}