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Tytuł pozycji:

BYSTANDER WI-38 CELLS MODULATE DNA DOUBLE-STRAND BREAK REPAIR IN MICROBEAM-TARGETED A549 CELLS THROUGH GAP JUNCTION INTERCELLULAR COMMUNICATION.

Tytuł :
BYSTANDER WI-38 CELLS MODULATE DNA DOUBLE-STRAND BREAK REPAIR IN MICROBEAM-TARGETED A549 CELLS THROUGH GAP JUNCTION INTERCELLULAR COMMUNICATION.
Autorzy :
Kobayashi A; SPICE-BIO research core, International Open Laboratory, National Institute of Radiological Sciences, National Institutes for Quantum and Radiological Science and Technology, Anagawa 4-9-1, Inage-ku, Chiba, Japan.; Graduate School of Comprehensive Human Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan.
Autsavapromporn N; SPICE-BIO research core, International Open Laboratory, National Institute of Radiological Sciences, National Institutes for Quantum and Radiological Science and Technology, Anagawa 4-9-1, Inage-ku, Chiba, Japan.; Division of Therapeutic Radiology and Oncology, Department of Radiology, Faculty of Medicine, Chiang Mai University, Thailand.
Ahmad TAFT; SPICE-BIO research core, International Open Laboratory, National Institute of Radiological Sciences, National Institutes for Quantum and Radiological Science and Technology, Anagawa 4-9-1, Inage-ku, Chiba, Japan.; Division of Agrotechnology and Biosciences, Malaysian Nuclear Agency, Bangi, Kajang, Malaysia.
Oikawa M; SPICE-BIO research core, International Open Laboratory, National Institute of Radiological Sciences, National Institutes for Quantum and Radiological Science and Technology, Anagawa 4-9-1, Inage-ku, Chiba, Japan.
Homma-Takeda S; SPICE-BIO research core, International Open Laboratory, National Institute of Radiological Sciences, National Institutes for Quantum and Radiological Science and Technology, Anagawa 4-9-1, Inage-ku, Chiba, Japan.
Furusawa Y; SPICE-BIO research core, International Open Laboratory, National Institute of Radiological Sciences, National Institutes for Quantum and Radiological Science and Technology, Anagawa 4-9-1, Inage-ku, Chiba, Japan.
Wang J; Key Laboratory of Ion Beam Bioengineering, Hefei Institute of Physical Science, Chinese Academy of Sciences and Anhui Province, No. 350 of Shushanhu Road, Hefei, PR China.
Konishi T; SPICE-BIO research core, International Open Laboratory, National Institute of Radiological Sciences, National Institutes for Quantum and Radiological Science and Technology, Anagawa 4-9-1, Inage-ku, Chiba, Japan.
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Źródło :
Radiation protection dosimetry [Radiat Prot Dosimetry] 2019 May 01; Vol. 183 (1-2), pp. 142-146.
Typ publikacji :
Journal Article
Język :
English
Imprint Name(s) :
Publication: 2004- : Oxford, UK : Oxford University Press
Original Publication: Ashford, Kent : Nuclear Technology Pub., c1981-
MeSH Terms :
A549 Cells/*radiation effects
Cell Communication/*radiation effects
DNA Breaks, Double-Stranded/*radiation effects
Gap Junctions/*radiation effects
Lung Neoplasms/*radiotherapy
Tumor Cells, Cultured/*radiation effects
Bystander Effect/radiation effects ; Cells, Cultured/radiation effects ; Coculture Techniques ; DNA Repair ; Fibroblasts/radiation effects ; Histones/analysis ; Humans ; Protons
Substance Nomenclature :
0 (Histones)
0 (Protons)
Entry Date(s) :
Date Created: 20181212 Date Completed: 20190604 Latest Revision: 20190604
Update Code :
20201020
DOI :
10.1093/rpd/ncy249
PMID :
30535060
Czasopismo naukowe
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.
(© The Author(s) 2018. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

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