ArticleOncogene2022
MMP-9 drives the melanomagenic transcription program through histone H3 tail proteolysis.
Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 45 citations in OpenAlex.
- B1486 is a highly potent VprBP inhibitor capable of blocking osteoclast differentiation and bone resorption.The Journal of biological chemistry · 2026Article
- VprBP drives prostate tumorigenesis by its kinase activity targeting histone H2A.Cell communication and signaling : CCS · 2026Article
- HDAC1 has intrinsic protease activity and regulates transcription through clipping histone H3 N-terminal tail.Cell death and differentiation · 2026Article
- ZDHHC4-mediated ZEB-2 S-palmitoylation promotes melanoma epithelial-mesenchymal transition via deubiquitinating and stabilizing ZEB-2.Cellular and molecular life sciences : CMLS · 2026Article
- Epigenetics of Malignant Melanoma: Mechanisms, Diagnostic Approaches and Therapeutic Applications.Oncology research · 2026Review
- Targeting Neuronal Nitric Oxide Synthase (nNOS) as a Novel Approach to Enhancing the Anti-Melanoma Activity of Immune Checkpoint Inhibitors.Pharmaceutics · 2025Article
- VprBP regulates osteoclast differentiation via an epigenetic mechanism involving histone H2A phosphorylation.Epigenetics & chromatin · 2024Article
- Histone Tail Cleavage as a Mechanism for Epigenetic Regulation.International journal of molecular sciences · 2024Review
- Mediator complex subunit 1 promotes oral squamous cell carcinoma progression by activating MMP9 transcription and suppressing CD8Journal of experimental & clinical cancer research : CR · 2024Article
- MMP-9-dependent proteolysis of the histone H3 N-terminal tail: a critical epigenetic step in driving oncogenic transcription and colon tumorigenesis.Molecular oncology · 2024Article
- The role of SWI/SNF complexes in digestive system neoplasms.Medical oncology (Northwood, London, England) · 2024Review
- Redefining metalloproteases specificity through network proteolysis.Trends in molecular medicine · 2024Review
- Exogenous recombinant N-acetylgalactosamine-4-sulfatase (Arylsulfatase B; ARSB) inhibits progression of B16F10 cutaneous melanomas and modulates cell signaling.Biochimica et biophysica acta. Molecular basis of disease · 2024Article
- VprBP/DCAF1 Triggers Melanomagenic Gene Silencing through Histone H2A Phosphorylation.Biomedicines · 2023Article
- The MMP-2 histone H3 N-terminal tail protease is selectively targeted to the transcription start sites of active genes.Epigenetics & chromatin · 2023Article
- The micronuclear histone H3 clipping in the unicellular eukaryoteMarine life science & technology · 2022Review
- Novel Roles of MT1-MMP and MMP-2: Beyond the Extracellular Milieu.International journal of molecular sciences · 2022Review
- Identification of Novel Natural Product Inhibitors against Matrix Metalloproteinase 9 Using Quantum Mechanical Fragment Molecular Orbital-Based Virtual Screening Methods.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Melanoma is a type of skin cancer that develops in pigment-producing melanocytes and often spreads to other parts of the body. Aberrant gene expression has been considered as a crucial step for increasing the risk of melanomagenesis, but how chromatin reorganization contributes to this pathogenic process is still not well understood. Here we report that matrix metalloproteinase 9 (MMP-9) localizes to the nucleus of melanoma cells and potentiates gene expression by proteolytically clipping the histone H3 N-terminal tail (H3NT). From genome-wide studies, we discovered that growth-regulatory genes are selectively targeted and activated by MMP-9-dependent H3NT proteolysis in melanoma cells. MMP-9 cooperates functionally with p300/CBP because MMP-9 cleaves H3NT in a manner that is dependent on p300/CBP-mediated acetylation of H3K18. The functional significance of MMP-9-dependent H3NT proteolysis is further underscored by the fact that RNAi knockdown and small-molecule inhibition of MMP-9 and p300/CBP impede melanomagenic gene expression and melanoma tumor growth. Together, our data establish new functions and mechanisms for nuclear MMP-9 in promoting melanomagenesis and demonstrate how MMP-9-dependent H3NT proteolysis can be exploited to prevent and treat melanoma skin cancer.
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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.