ArticleScientific reports2016
Function of high-mobility group A proteins in the DNA damage signaling for the induction of apoptosis.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- HMGA1 is associated with unfavorable outcome and accelerates the aggressiveness of cholangiocarcinoma.SAGE open medicine · 2026Article
- 3' UTR-truncated HMGA2 promotes erythroblasts production from human embryonic stem cells.Stem cells translational medicine · 2025Article
- Parkinson's Disease and MicroRNAs: A Duel Between Inhibition and Stimulation of Apoptosis in Neuronal Cells.Molecular neurobiology · 2024Review
- Decoding high mobility group A2 protein expression regulation and implications in human cancers.Discover oncology · 2024Review
- FANCD2 counteracts OMolecular biology reports · 2024Article
- The landscape of SETBP1 gene expression and transcription factor activity across human tissues.PloS one · 2024Article
- HMGA1 and FOXM1 Cooperate to Promote G2/M Cell Cycle Progression in Cancer Cells.Life (Basel, Switzerland) · 2023Article
- Nuclear High Mobility Group A2 (HMGA2) Interactome Revealed by Biotin Proximity Labeling.International journal of molecular sciences · 2023Article
- Review
- HMGA2-mediated tumorigenesis through angiogenesis in leiomyoma.Fertility and sterility · 2020Article
- NFAT5, which protects against hypertonicity, is activated by that stress via structuring of its intrinsically disordered domain.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- High Mobility Group AT-Hook 2 (HMGA2) Oncogenicity in Mesenchymal and Epithelial Neoplasia.International journal of molecular sciences · 2020Review
- SMARCAD1-mediated recruitment of the DNA mismatch repair protein MutLα to MutSα on damaged chromatin induces apoptosis in human cells.The Journal of biological chemistry · 2020Article
- A novel role of Krüppel-like factor 8 as an apoptosis repressor in hepatocellular carcinoma.Cancer cell international · 2020Article
- HIT000218960 promotes gastric cancer cell proliferation and migration through upregulation of HMGA2 expression.Oncology letters · 2019Article
- Impact of high-mobility-group A2 overexpression on epithelial-mesenchymal transition in pancreatic cancer.Cancer management and research · 2019Article
- The Prominent Role of HMGA Proteins in the Early Management of Gastrointestinal Cancers.BioMed research international · 2019Review
- Gene surgery: Potential applications for human diseases.EXCLI journal · 2019Review
- Specific binding of PCBP1 to heavily oxidized RNA to induce cell death.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- HMGA1 exacerbates tumor growth through regulating the cell cycle and accelerates migration/invasion via targeting miR-221/222 in cervical cancer.Cell death & disease · 2018Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
O(6)-Methylguanine produced in DNA can pair with thymine during DNA replication, thus leading to a G-to-A transition mutation. To prevent such outcomes, cells harboring O(6)-methylguanine-containing mispair undergo apoptosis that requires the function of mismatch repair (MMR) protein complex. To identify the genes involved in the induction of apoptosis, we performed gene-trap mutagenesis and isolated a clone of mouse cells exhibiting an increased resistance to the killing effect of an alkylating agent, N-methyl-N-nitrosourea (MNU). The mutant carries an insertion in the Hmga2 gene, which belongs to a gene family encoding the high-mobility group A non-histone chromatin proteins. To elucidate the function of HMGA proteins in the apoptosis pathway, we introduced siRNAs for HMGA1 and/or HMGA2 into human HeLa MR cells defective in O(6)-methylguanine-DNA methyltransferase. HMGA1- and HMGA2-single knockdown cells showed an increased resistance to MNU, and HMGA1/HMGA2-double knockdown cells exhibited further increased tolerance compared to the control. The phosphorylation of ATR and CHK1, the appearance of a sub-G1 population, and caspase-9 activation were suppressed in the knockdown cells, although the formation of mismatch recognition complex was unaffected. These results suggest that HMGA family proteins function at the step following the damage recognition in the process of apoptosis triggered by O(6)-methylguanine.
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