ArticleScientific reports2018
Evidence for a radiation-responsive 'p53 gateway' contributing significantly to the radioresistance of lepidopteran insect cells.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 242 citations in OpenAlex.
- Mitochondrial Dysfunction Predisposes Radioresistant Insect Cells to Ionizing Radiation by Impairing DNA Repair.Cell biochemistry and biophysics · 2026Article
- On the Boundary of Exploratory Genomics and Translation in Sequential Glioblastoma.International journal of molecular sciences · 2024Article
- Impact ofJournal of radiosurgery and SBRT · 2024Article
- Relationship between p53 status and the bioeffect of ionizing radiation.Oncology letters · 2021Review
- The Benefit of Reactivating p53 under MAPK Inhibition on the Efficacy of Radiotherapy in Melanoma.Cancers · 2019Article
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recently, we have demonstrated that microRNA-31 (miR-31) overexpression is inherent to radiation-induced cell death in the highly radioresistant Sf9 insect cells, and regulates pro-apoptotic Bax translocation to mitochondria. In the present study, we report that at sub-lethal radiation doses for Sf9 cells, miR-31 is significantly downregulated and is tightly regulated by an unusual mechanism involving p53. While ectopic overexpression of a well-conserved Sfp53 caused typical apoptosis, radiation-induced p53 accumulation observed selectively at sub-lethal doses failed to induce cell death. Further investigation of this paradoxical response revealed an intriguing phenomenon that sub-lethal radiation doses result in accumulation of a 'hyper-phosphorylated' Sfp53, which in turn binds to miR-31 genomic location and suppresses its expression to prevent cell death. Interestingly, priming cells with sub-lethal doses even prevented the apoptosis induced by lethal radiation or ectopic Sfp53 overexpression. On the other hand, silencing p53 increased radiation-induced cell death by inhibiting miR-31 downregulation. This study thus shows the existence of a unique radiation-responsive 'p53 gateway' preventing miR-31-mediated apoptosis in Sf9 cells. Since Sfp53 has a good functional homology with human p53, this study may have significant implications for effectively modulating the mammalian cell radioresistance.
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