Please use this identifier to cite or link to this item: http://cmuir.cmu.ac.th/jspui/handle/6653943832/65633
Title: BYSTANDER WI-38 CELLS MODULATE DNA DOUBLE-STRAND BREAK REPAIR IN MICROBEAM-TARGETED A549 CELLS THROUGH GAP JUNCTION INTERCELLULAR COMMUNICATION
Authors: A. Kobayashi
N. Autsavapromporn
T. A.F.Tengku Ahmad
M. Oikawa
S. Homma-Takeda
Y. Furusawa
J. Wang
T. Konishi
Keywords: Health Professions
Medicine
Physics and Astronomy
Issue Date: 1-May-2019
Abstract: © The Author(s) 2018. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com. 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.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85066239560&origin=inward
http://cmuir.cmu.ac.th/jspui/handle/6653943832/65633
ISSN: 17423406
Appears in Collections:CMUL: Journal Articles

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