ArticleOncogene2009
Matrix Metalloproteinase-9 gene induction by a truncated oncogenic NF-kappaB2 protein involves the recruitment of MLL1 and MLL2 H3K4 histone methyltransferase complexes.
Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 36 citations in OpenAlex.
- Therapeutic implications of epigenetic alterations in burns: a new frontier in burn medicine.Clinical science (London, England : 1979) · 2026Review
- Epigenetics and diabetic wound healing: Wilms tumor 1-associated protein as a therapeutic target.World journal of diabetes · 2025Article
- Histone modifications and their roles in macrophage-mediated inflammation: a new target for diabetic wound healing.Frontiers in immunology · 2024Review
- Evolving spectrum of diabetic wound: Mechanistic insights and therapeutic targets.World journal of diabetes · 2022Review
- Macrophage Phenotypes in Normal and Diabetic Wound Healing and Therapeutic Interventions.Cells · 2022Review
- Article
- Targeting matrix metallopeptidase 2 by hydroxyurea selectively kills acute myeloid mixed-lineage leukemia.Cell death discovery · 2022Article
- Changes in histone H3 lysine 4 trimethylation in Hashimoto's thyroiditis.Archives of medical science : AMS · 2022Article
- ASB2 is a direct target of FLI1 that sustains NF-κB pathway activation in germinal center-derived diffuse large B-cell lymphoma.Journal of experimental & clinical cancer research : CR · 2021Article
- lncRNA MIAT promotes cell invasion and migration in esophageal cancer.Experimental and therapeutic medicine · 2020Article
- Epigenetic Regulation of TLR4 in Diabetic Macrophages Modulates Immunometabolism and Wound Repair.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Sepsis Induces Prolonged Epigenetic Modifications in Bone Marrow and Peripheral Macrophages Impairing Inflammation and Wound Healing.Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- Targeting epigenetic mechanisms in diabetic wound healing.Translational research : the journal of laboratory and clinical medicine · 2019Review
- Article
- Role of PARP-1 as a novel transcriptional regulator of MMP-9 in diabetic retinopathy.Biochimica et biophysica acta. Molecular basis of disease · 2017Article
- Thrombin-induced, TNFR-dependent miR-181c downregulation promotes MLL1 and NF-κB target gene expression in human microglia.Journal of neuroinflammation · 2017Article
- MKL1 potentiates lung cancer cell migration and invasion by epigenetically activating MMP9 transcription.Oncogene · 2015Article
- Sirt1, a negative regulator of matrix metalloproteinase-9 in diabetic retinopathy.Investigative ophthalmology & visual science · 2014Article
- MDM2 restrains estrogen-mediated AKT activation by promoting TBK1-dependent HPIP degradation.Cell death and differentiation · 2014Article
- Downregulation of RUNX1/CBFβ by MLL fusion proteins enhances hematopoietic stem cell self-renewal.Blood · 2014Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Constitutive nuclear factor (NF)-kappaB activation in haematological malignancies is caused in several cases by loss of function mutations within the coding sequence of NF-kappaB inhibitory molecules such as IkappaBalpha or p100. Hut-78, a truncated form of p100, constitutively generates p52 and contributes to the development of T-cell lymphomas but the molecular mechanism underlying this oncogenic potential remains unclear. We show here that MMP9 gene expression is induced through the alternative NF-kappaB-activating pathway in fibroblasts and also on Hut-78 or p52 overexpression in fibroblasts as well as in lymphoma cells. p52 is critical for Hut-78-mediated MMP9 gene induction as a Hut-78 mutant as well as other truncated NF-kappaB2 proteins that are not processed into p52 failed to induce the expression of this metalloproteinase. Conversely, MMP9 gene expression is impaired in p52-depleted HUT-78 cells. Interestingly, MLL1 and MLL2 H3K4 methyltransferase complexes are tethered by p52 on the MMP9 but not on the IkappaBalpha promoter, and the H3K4 trimethyltransferase activity recruited on the MMP9 promoter is impaired in p52-depleted HUT-78 cells. Moreover, MLL1 and MLL2 are associated with Hut-78 in a native chromatin-enriched extract. Thus, we identified a molecular mechanism by which the recruitment of a H3K4 histone methyltransferase complex on the promoter of a NF-kappaB-dependent gene induces its expression and potentially the invasive potential of lymphoma cells harbouring constitutive activity of the alternative NF-kappaB-activating pathway.
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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.