ArticleAntioxidants (Basel, Switzerland)2022
Golgi Phosphoprotein 3 Mediates Radiation-Induced Bystander Effect via ERK/EGR1/TNF-α Signal Axis.
Article in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Reprogrammed MDSCs promote Th1-dominant antitumour response via CD40 induced by autocrine TNF-α after combining cryo-thermal therapy with IL6 and IL17A neutralization.Clinical and translational medicine · 2025Article
- Isoliquiritigenin alleviates radiation-induced intestinal injury in lung cancer by inhibiting TNF-α/caspase3 signaling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Microgravity alleviates low-dose radiation-induced non-targeted carcinogenic effects.NPJ microgravity · 2025Article
- Transcriptional Regulators in the Cerebellum in Chronic Schizophrenia: Novel Possible Targets for Pharmacological Interventions.International journal of molecular sciences · 2025Article
- Low-Dose Non-Targeted Effects and Mitochondrial Control.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
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-α 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-α and determine the level of released TNF-α. Our findings provide new insights into the molecular mechanism of the RIBE and a potential target for RIBE modulation.
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Registered trials
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