ArticleRadiation oncology (London, England)2014
RAD9 deficiency enhances radiation induced bystander DNA damage and transcriptomal response.
Article in Radiation oncology (London, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- NUPR1 in breast cancer: mechanisms and potential applications.Frontiers in physiology · 2026Review
- Serum miRNA and Metabolomic Signatures of Residential Radon Exposure in Chiang Mai, Thailand.Toxics · 2025Article
- The transcriptomic revolution and radiation biology.International journal of radiation biology · 2022Article
- NUPR1 is a critical repressor of ferroptosis.Nature communications · 2021Article
- Investigation of the Possible Role of RAD9 in Post-Diapaused Embryonic Development of the Brine ShrimpGenes · 2019Article
- Article
- Changes in gene expression as one of the key mechanisms involved in radiation-induced bystander effect.Biomedical reports · 2018Review
- In vivo Exposure Effects ofAsia Oceania journal of nuclear medicine & biology · 2018Article
- Article
- Bystander autophagy mediated by radiation-induced exosomal miR-7-5p in non-targeted human bronchial epithelial cells.Scientific reports · 2016Article
- Transcription Factors in the Cellular Response to Charged Particle Exposure.Frontiers in oncology · 2016Review
- Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundRadiation induced bystander effects are an important component of the overall response of cells to irradiation and are associated with human health risks. The mechanism responsible includes intra-cellular and inter-cellular signaling by which the bystander response is propagated. However, details of the signaling mechanism are not well defined.
methodsWe measured the bystander response of Mrad9+/+ and Mrad9-/- mouse embryonic stem cells, as well as human H1299 cells with inherent or RNA interference-mediated reduced RAD9 levels after exposure to 1 Gy α particles, by scoring chromosomal aberrations and micronuclei formation, respectively. In addition, we used microarray gene expression analyses to profile the transcriptome of directly irradiated and bystander H1299 cells.
resultsWe demonstrated that Mrad9 null enhances chromatid aberration frequency induced by radiation in bystander mouse embryonic stem cells. In addition, we found that H1299 cells with reduced RAD9 protein levels showed a higher frequency of radiation induced bystander micronuclei formation, compared with parental cells containing inherent levels of RAD9. The enhanced bystander response in human cells was associated with a unique transcriptomic profile. In unirradiated cells, RAD9 reduction broadly affected stress response pathways at the mRNA level; there was reduction in transcript levels corresponding to genes encoding multiple members of the UVA-MAPK and p38MAPK families, such as STAT1 and PARP1, suggesting that these signaling mechanisms may not function optimally when RAD9 is reduced. Using network analysis, we found that differential activation of the SP1 and NUPR1 transcriptional regulators was predicted in directly irradiated and bystander H1299 cells. Transcription factor prediction analysis also implied that HIF1α (Hypoxia induced factor 1 alpha) activation by protein stabilization in irradiated cells could be a negative predictor of the bystander response, suggesting that local hypoxic stress experienced by cells directly exposed to radiation may influence whether or not they will elicit a bystander response in neighboring cells.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.