Enhanced DNA double-strand break repair of microbeam targeted A549 lung carcinoma cells by adjacent WI38 normal lung fibroblast cells via bidirectional signaling

doi:10.1016/j.mrfmmm.2017.06.006

CORC > 合肥物质科学研究院 > 中国科学院合肥物质科学研究院 > 技术生物与农业工程研究所

	Enhanced DNA double-strand break repair of microbeam targeted A549 lung carcinoma cells by adjacent WI38 normal lung fibroblast cells via bidirectional signaling
	Kobayashi, Alisa 1,2,3; Farizal Tengku Ahmad, Tengku Ahbrizal 1,4; Autsavapromporn, Narongchai 1,5; Oikawa, Masakazu 1,2; Homma-Takeda, Shino 6; Furusawa, Yoshiya 1,6; Wang, Jun1,7 ; Konishi, Teruaki 1,6
刊名	MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS
	2017-10-01
卷号	803 期号:无页码:1-8
关键词	Proton Microbeam Lung Cells Gamma-h2ax Radiation Induced Bystander Effect Rescue Effect
DOI	10.1016/j.mrfmmm.2017.06.006
文献子类	Article
英文摘要	Understanding the mechanisms underlying the radiation-induced bystander effect (RIBE) and bi-directional signaling between irradiated carcinoma cells and their surrounding non-irradiated normal cells is relevant to cancer radiotherapy. The present study investigated propagation of RIBE signals between human lung carcinoma A549 cells and normal lung fibroblast WI38 cells in bystander cells, either directly or indirectly contacting irradiated A549 cells. We prepared A549-GFP/WI38 co-cultures and A549-GFP/A549 co-cultures, in which A549-GFP cells stably expressing H2BGFP were co-cultured with either A549 cells or WI38 cells, respectively. Using the SPICE-NIRS microbeam, only the A549-GFP cells were irradiated with 500 protons per cell. The level of gamma-H2AX, a marker for DNA double-strand breaks (DSB), was subsequently measured for up to 24 h postirradiation in three categories of cells: (1) "targeted"/irradiated A549-GFP cells; (2) "neighboring"/non-irradiated cells directly contacting the "targeted" cells; and (3) "distant"/non-irradiated cells, which were not in direct contact with the "targeted" cells. We found that DSB repair in targeted A549-GFP cells was enhanced by co-cultured WI38 cells. The bystander response in A549-GFP/A549 cell co-cultures, as marked by gamma-H2AX levels at 8 h post-irradiation, showed a decrease to non-irradiated control level when approaching 24 h, while the neighboring/distant bystander WI38 cells in A549-GFP/WI38 co-cultures was maintained at a similar level until 24 h post-irradiation. Surprisingly, distant A549-GFP cells in A549-GFP/WI38 co-cultures showed time dependency similar to bystander WI38 cells, but not to distant cells in A549-GFP/A549 co-cultures. These observations indicate that gamma-H2AX was induced in WI38 cells as a result of RIBE. WI38 cells were not only involved in rescue of targeted A549, but also in the modification of RIBE against distant A549-GFP cells. The present results demonstrate that radiation-induced bi-directional signaling had extended a profound influence on cellular sensitivity to radiation as well as the sensitivity to RIBE.
WOS关键词	CARBON ION RADIOTHERAPY ; ALPHA-PARTICLES ; CANCER-CELLS ; STEM-LIKE ; X-RAYS ; BYSTANDER ; RADIATION ; IRRADIATION ; COMMUNICATION ; MODULATION
WOS研究方向	Biotechnology & Applied Microbiology ; Genetics & Heredity ; Toxicology
语种	英语
WOS记录号	WOS:000413598800001
资助机构	JSPS KAKENHI(25861137) ; JSPS KAKENHI(25861137) ; JSPS KAKENHI(25861137) ; JSPS KAKENHI(25861137) ; NIRS-Sharing of advanced research infrastructure(S13-TK01 ; NIRS-Sharing of advanced research infrastructure(S13-TK01 ; NIRS-Sharing of advanced research infrastructure(S13-TK01 ; NIRS-Sharing of advanced research infrastructure(S13-TK01 ; S16-AK01) ; S16-AK01) ; S16-AK01) ; S16-AK01) ; JSPS KAKENHI(25861137) ; JSPS KAKENHI(25861137) ; JSPS KAKENHI(25861137) ; JSPS KAKENHI(25861137) ; NIRS-Sharing of advanced research infrastructure(S13-TK01 ; NIRS-Sharing of advanced research infrastructure(S13-TK01 ; NIRS-Sharing of advanced research infrastructure(S13-TK01 ; NIRS-Sharing of advanced research infrastructure(S13-TK01 ; S16-AK01) ; S16-AK01) ; S16-AK01) ; S16-AK01)
内容类型	期刊论文
源URL	[http://ir.hfcas.ac.cn:8080/handle/334002/33809]
专题	合肥物质科学研究院_技术生物与农业工程研究所
作者单位	1.Natl Inst Quantum & Radiol Sci & Technol, Natl Inst Radiol Sci, NIRS Int Open Lab, SPICE BIO Res Core,Inage Ku, Anagawa 4-9-1, Chiba 2638555, Japan 2.Natl Inst Quantum & Radiol Sci & Technol, Natl Inst Radiol Sci, Dept Accelerator & Med Phys, Inage Ku, Anagawa 4-9-1, Chiba 2638555, Japan 3.Univ Tsukuba, Grad Sch Comprehens Human Sci, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan 4.Agensi Nuklear Malaysia, Div Agrotechnol & Biosci, Bangi 43000, Kajang, Malaysia 5.Chiang Mai Univ, Div Therapeut Radiol & Oncol, Dept Radiol, Fac Med, Chiang Mai, Thailand 6.Natl Inst Quantum & Radiol Sci & Technol, Natl Inst Radiol Sci, Dept Basic Med Sci Radiat Damages, Inage Ku, Anagawa 4-9-1, Chiba 2638555, Japan 7.Chinese Acad Sci & Anhui Prov, Hefei Inst Phys Sci, Key Lab Ion Beam Bioengn, 350 Shushanhu Rd, Hefei 230031, Anhui, Peoples R China
推荐引用方式 GB/T 7714	Kobayashi, Alisa,Farizal Tengku Ahmad, Tengku Ahbrizal,Autsavapromporn, Narongchai,et al. Enhanced DNA double-strand break repair of microbeam targeted A549 lung carcinoma cells by adjacent WI38 normal lung fibroblast cells via bidirectional signaling[J]. MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS,2017,803(无):1-8.
APA	Kobayashi, Alisa.,Farizal Tengku Ahmad, Tengku Ahbrizal.,Autsavapromporn, Narongchai.,Oikawa, Masakazu.,Homma-Takeda, Shino.,...&Konishi, Teruaki.(2017).Enhanced DNA double-strand break repair of microbeam targeted A549 lung carcinoma cells by adjacent WI38 normal lung fibroblast cells via bidirectional signaling.MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS,803(无),1-8.
MLA	Kobayashi, Alisa,et al."Enhanced DNA double-strand break repair of microbeam targeted A549 lung carcinoma cells by adjacent WI38 normal lung fibroblast cells via bidirectional signaling".MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS 803.无(2017):1-8.