Abstract:
: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, which 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, inhibition of gap junction intercellular communication (GJIC) attenuated DSB repair in targeted A549-GFP cells, and suppressed RIBE in bystander WI-38 cells but not in distant A549-GFP cells. This suggests that GJIC plays a two-way role through propagating DNA damage effect between carcinoma to normal cells and reversing the bystander signaling, also called 'rescue effect' from bystander cells to irradiated cells, to enhance the DSB repair in targeted cells.
journal_name
Radiat Prot Dosimetryjournal_title
Radiation protection dosimetryauthors
Kobayashi A,Autsavapromporn N,Ahmad TAFT,Oikawa M,Homma-Takeda S,Furusawa Y,Wang J,Konishi Tdoi
10.1093/rpd/ncy249subject
Has Abstractpub_date
2019-05-01 00:00:00pages
142-146issue
1-2eissn
0144-8420issn
1742-3406pii
5238185journal_volume
183pub_type
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journal_title:Radiation protection dosimetry
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journal_title:Radiation protection dosimetry
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journal_title:Radiation protection dosimetry
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journal_title:Radiation protection dosimetry
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journal_title:Radiation protection dosimetry
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journal_title:Radiation protection dosimetry
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journal_title:Radiation protection dosimetry
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journal_title:Radiation protection dosimetry
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