ArticleRNA biology2012
miR-3928 activates ATR pathway by targeting Dicer.
Article in RNA biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
- FLASH Radiotherapy: Benefits, Mechanisms, and Obstacles to Its Clinical Application.International journal of molecular sciences · 2024Review
- Article
- MicroRNA induction by copy number gain is associated with poor outcome in squamous cell carcinoma of the lung.Scientific reports · 2018Article
- Targeting MicroRNAs in Prostate Cancer Radiotherapy.Theranostics · 2017Review
- Dicer interacts with SIRT7 and regulates H3K18 deacetylation in response to DNA damaging agents.Nucleic acids research · 2016Article
- Down-regulation of BTG1 by miR-454-3p enhances cellular radiosensitivity in renal carcinoma cells.Radiation oncology (London, England) · 2014Article
- Mutant p53 regulates Dicer through p63-dependent and -independent mechanisms to promote an invasive phenotype.The Journal of biological chemistry · 2014Article
- MiR-21 is involved in radiation-induced bystander effects.RNA biology · 2014Article
- MicroRNAs in the DNA Damage/Repair Network and Cancer.International journal of genomics · 2014Review
- Repression of ATR pathway by miR-185 enhances radiation-induced apoptosis and proliferation inhibition.Cell death & disease · 2013Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alterations in microRNA (miRNA) expression have been observed in cells subjected to exogenous stresses, implying that miRNAs play an important role in cellular stress response; however, the underlying mechanism is still largely unknown. In the present study, we found that miR-3928 was implicated in cellular response to ionizing radiation. After exposed to X-rays, miR-3928 expression increased in 1.5 h and then decreased, meanwhile Dicer, a key component in the miRNA processing machinery, increased gradually. An oscillation was observed in the expression of both mature miR-3928 and Dicer mRNA from 2 h to 3.5 h in irradiated cells. Then, we verified that miR-3928 directly bound to the 3'-untranslated region of Dicer mRNA. Consequently, Dicer expression was suppressed and the maturation of other miRNAs including miR-185, miR-300, and miR-663, was inhibited. Overexpression of miR-3928 induced DNA damage, activated ATR, and phosphorylated Chk1 accompanied by G1 arrest. Taken together, these findings replenished ATR/Chk1 pathway by revealing a novel miRNA regulatory network in response to exogenous stress, in which miR-3928 plays an important role in regulating the expression of Dicer.
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Registered trials
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.