ArticleCell death & disease2013
Mutual regulation between DNA-PKcs and Snail1 leads to increased genomic instability and aggressive tumor characteristics.
Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
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
26 citing papers in PubMed, 34 citations in OpenAlex.
- C/EBPγ induces epithelial-mesenchymal transition and facilitates DNA double-strand break repair in lung adenocarcinoma cells.Cell death discovery · 2026Article
- A clinically concordant vulvar cancer patient-derived xenograft model retaining primary molecular signature for preclinical drug sensitivity assessment.Open medicine (Warsaw, Poland) · 2026Article
- MSK1 promotes colorectal cancer metastasis by increasing Snail protein stability through USP5-mediated Snail deubiquitination.Experimental & molecular medicine · 2025Article
- DNA-PKcs, a player winding and dancing with RNA metabolism and diseases.Cellular & molecular biology letters · 2025Review
- Triple-Negative Breast Cancer Progression and Drug Resistance in the Context of Epithelial-Mesenchymal Transition.Cancers · 2025Review
- Control of Snail1 protein stability by post-translational modifications: the basis for a complex regulation of Snail1 function.International journal of biological sciences · 2025Review
- Disruption of RNA Splicing Increases Vulnerability of Cells to DNA-PK Inhibitors.International journal of molecular sciences · 2024Article
- Secrets of DNA-PKcs beyond DNA repair.NPJ precision oncology · 2024Review
- DNA-PKcs/AKT1 inhibits epithelial-mesenchymal transition during radiation-induced pulmonary fibrosis by inducing ubiquitination and degradation of Twist1.Clinical and translational medicine · 2024Article
- ERK3 Increases Snail Protein Stability by Inhibiting FBXO11-Mediated Snail Ubiquitination.Cancers · 2023Article
- Regulation of DNA-PK activity promotes the progression of TNBC via enhancing the immunosuppressive function of myeloid-derived suppressor cells.Cancer medicine · 2023Article
- Human Cytomegalovirus Induces Vitamin-D Resistance In Vitro by Dysregulating the Transcriptional Repressor Snail.Viruses · 2022Article
- Role of EMT in the DNA damage response, double-strand break repair pathway choice and its implications in cancer treatment.Cancer science · 2022Review
- Epigenetic Regulation and Post-Translational Modifications of SNAI1 in Cancer Metastasis.International journal of molecular sciences · 2021Review
- Niclosamide and Pyrvinium Are Both Potential Therapeutics for Osteosarcoma, Inhibiting Wnt-Axin2-Snail Cascade.Cancers · 2021Article
- E2A Modulates Stemness, Metastasis, and Therapeutic Resistance of Breast Cancer.Cancer research · 2021Article
- CRL4AOncogene · 2021Article
- STK39 promotes breast cancer invasion and metastasis by increasing SNAI1 activity upon phosphorylation.Theranostics · 2021Article
- Pleiotropic Impact of DNA-PK in Cancer and Implications for Therapeutic Strategies.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019Article
- Snail1: A Transcriptional Factor Controlled at Multiple Levels.Journal of clinical medicine · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although the roles of DNA-dependent protein kinase catalytic subunits (DNA-PKcs) in the non-homologous end joining (NHEJ) of DNA repair are well-recognized, the biological mechanisms and regulators by DNA-PKcs besides DNA repair, have not been clearly described. Here, we show that active DNA-PKcs caused by ionizing radiation, phosphorylated Snail1 at serine (Ser) 100, led to increased Snail1 stability. Furthermore, phosphorylated Snail1 at Ser100 reciprocally inhibited the kinase activity of DNA-PKcs, resulting in an inhibition of DNA repair activity. Moreover, Snail1 phosphorylation by DNA-PKcs was involved in genomic instability and aggressive tumor characteristics. Our results describe novel cellular mechanisms that affect genomic instability, sensitivity to DNA-damaging agents, and the migration of tumor cells by reciprocal regulation between DNA-PKcs and Snail1.
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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.