Presentation Bystander WI-38 normal lung fibroblast cells modulate DNA double-strand break repair in microbeam-targeted A549 cells through gap junction intercellular communication

Kobayashi, Alisa  ,  Autsavapromporn, Narongchai  ,  Ahbrizal Farizal Tengku Ahmad, Tengku  ,  Oikawa, Masakazu  ,  Shino, Homma-Takeda  ,  Furusawa, Yoshiya  ,  Wang, Jun  ,  Konishi, Teruaki

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

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