Golgi Phosphoprotein 3 Mediates Radiation-Induced Bystander Effect via ERK/EGR1/TNF-alpha Signal Axis
文献类型： 外文期刊
作者： Qin, Feng 1 ; Chen, Guodong 1 ; Yu, Kwan Ngok 5 ; Yang, Miaomiao 1 ; Cao, Wei 1 ; Kong, Peizhong 1 ; Peng, Shengjie 1 ; Sun, Mingyu 1 ; Nie, Lili 1 ; Han, Wei 1 ;
作者机构： 1.Chinese Acad Sci, Inst Hlth & Med Technol, Hefei Inst Phys Sci, Anhui Prov Key Lab Med Phys & Technol, Hefei 230031, Peoples R China
2.USTC, Grad Sch, Scinece Isl Branch, Hefei 230026, Peoples R China
3.Anhui Acad Agr Sci, Inst Sericultural, Hefei 230061, Peoples R China
4.Chinese Acad Sci, Hefei Canc Hosp, Hefei 230031, Peoples R China
5.City Univ Hong Kong, Dept Phys, Kowloon Tong, Tat Chee Ave, Hong Kong 999077, Peoples R China
6.City Univ Hong Kong, State Key Lab Marine Pollut, Kowloon Tong, Tat Chee Ave, Hong Kong 999077, Peoples R China
7.Soochow Univ, Collaborat Innovat Ctr Radiat Med, Jiangsu Higher Educ Inst, Suzhou 215006, Peoples R China
8.Soochow Univ, Sch Radiol & Interdisciplinary Sci RAD X, Suzhou 215006, Peoples R China
关键词： GOLPH3; radiation-induced bystander effect; TNF-alpha; EGR1
期刊名称：ANTIOXIDANTS （ 影响因子：7.675； 五年影响因子：7.886 ）
ISSN：
年卷期： 2022 年 11 卷 11 期
页码：
收录情况： SCI
摘要： The radiation-induced bystander effect (RIBE), an important non-targeted effect of radiation, has been proposed to be associated with irradiation-caused secondary cancers and reproductive damage beyond the irradiation-treated area after radiotherapy. However, the mechanisms for RIBE signal(s) regulation and transduction are not well understood. In the present work, we found that a Golgi protein, GOLPH3, was involved in RIBE transduction. Knocking down GOLPH3 in irradiated cells blocked the generation of the RIBE, whereas re-expression of GOLPH3 in knockdown cells rescued the RIBE. Furthermore, TNF-alpha was identified as an important intercellular signal molecule in the GOLPH3-mediated RIBE. A novel signal axis, GOLPH3/ERK/EGR1, was discovered to modulate the transcription of TNF-alpha and determine the level of released TNF-alpha. Our findings provide new insights into the molecular mechanism of the RIBE and a potential target for RIBE modulation.
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