ArticleCancer research2009
Suppression of nonhomologous end joining repair by overexpression of HMGA2.
Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.
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- Effects of Differing Underlying Assumptions in In Silico Models on Predictions of DNA Damage and Repair.Radiation research · 2023Article
- TI17, a novel compound, exerts anti-MM activity by impairing Trip13 function of DSBs repair and enhancing DNA damage.Cancer medicine · 2023Article
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- Effects of HMGA2 on the epithelial-mesenchymal transition-related genes in ACHN renal cell carcinoma cells-derived xenografts in nude mice.BMC cancer · 2022Article
- Mechanistic Modelling of Slow and Fast NHEJ DNA Repair Pathways Following Radiation for G0/G1 Normal Tissue Cells.Cancers · 2021Article
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- Emerging roles for HMGA2 in colorectal cancer.Translational oncology · 2021Review
- MicroRNAs as Biomarkers for Early Diagnosis, Prognosis, and Therapeutic Targeting of Ovarian Cancer.Journal of oncology · 2021Review
- Dying tumor cell-derived exosomal miR-194-5p potentiates survival and repopulation of tumor repopulating cells upon radiotherapy in pancreatic cancer.Molecular cancer · 2020Article
- MiR-509-3 augments the synthetic lethality of PARPi by regulating HR repair in PDX model of HGSOC.Journal of hematology & oncology · 2020Article
- High Mobility Group A (HMGA): Chromatin Nodes Controlled by a Knotty miRNA Network.International journal of molecular sciences · 2020Review
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- MicroRNA Let-7d-3p Contributes to Cardiac Protection via Targeting HMGA2.International journal of molecular sciences · 2019Article
- Elevated TRIP13 drives cell proliferation and drug resistance in bladder cancer.American journal of translational research · 2019Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Understanding the molecular details associated with aberrant high mobility group A2 (HMGA2) gene expression is key to establishing the mechanism(s) underlying its oncogenic potential and effect on the development of therapeutic strategies. Here, we report the involvement of HMGA2 in impairing DNA-dependent protein kinase (DNA-PK) during the nonhomologous end joining (NHEJ) process. We showed that HMGA2-expressing cells displayed deficiency in overall and precise DNA end-joining repair and accumulated more endogenous DNA damage. Proper and timely activation of DNA-PK, consisting of Ku70, Ku80, and DNA-PKcs subunits, is essential for the repair of DNA double strand breaks (DSB) generated endogenously or by exposure to genotoxins. In cells overexpressing HMGA2, accumulation of histone 2A variant X phosphorylation at Ser-139 (gamma-H2AX) was associated with hyperphosphorylation of DNA-PKcs at Thr-2609 and Ser-2056 before and after the induction of DSBs. Also, the steady-state complex of Ku and DNA ends was altered by HMGA2. Microirradiation and real-time imaging in living cells revealed that HMGA2 delayed the release of DNA-PKcs from DSB sites, similar to observations found in DNA-PKcs mutants. Moreover, HMGA2 alone was sufficient to induce chromosomal aberrations, a hallmark of deficiency in NHEJ-mediated DNA repair. In summary, a novel role for HMGA2 to interfere with NHEJ processes was uncovered, implicating HMGA2 in the promotion of genome instability and tumorigenesis.
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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.