ArticleFrontiers in genetics2019
EZH2 Regulates Protein Stability via Recruiting USP7 to Mediate Neuronal Gene Expression in Cancer Cells.
Article in Frontiers in genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 58 citations in OpenAlex.
- Review
- Novel therapeutic targets at the crossroad between epigenetics and signal transduction pathways in B-cell lymphomas.Clinical and experimental medicine · 2026Review
- USP10 deubiquitinase: Physiological function, diseases and therapeutic target (Review).International journal of molecular medicine · 2026Review
- Histone methylation defines c-Jun/Sox2/Hif1α axis that controls stemness and tumor progression in squamous cell carcinoma.Nature communications · 2026Article
- BMSC-derived extracellular vesicles enhance osteosarcoma proliferation and metastasis via the circRNA-0010220/β-catenin pathway.Cell death & disease · 2026Article
- Understanding cancer as a systemic disease through comprehension of neural stemness as the core property of cancer cell and the basic rules it dictates.Frontiers in cell and developmental biology · 2026Review
- Protein Arginine Methyltransferases from Regulatory Function to Clinical Implication in Central Nervous System.Cellular and molecular neurobiology · 2025Review
- The multifaceted role of post-translational modifications of LSD1 in cellular processes and disease pathogenesis.Genes & diseases · 2025Review
- Inhibition of SCFCommunications biology · 2025Article
- Predictive modelling of acute Promyelocytic leukaemia resistance to retinoic acid therapy.Briefings in bioinformatics · 2024Article
- Lack of basic rationale in epithelial-mesenchymal transition and its related concepts.Cell & bioscience · 2024Review
- The CoREST complex regulates multiple histone modifications temporal-specifically in clock neurons.Open biology · 2024Article
- Epigenetic control and manipulation of neuronal maturation timing.Current opinion in genetics & development · 2024Review
- EZH2 is a key component of hepatoblastoma tumor cell growth.Pediatric blood & cancer · 2024Article
- Promoter hypermethylation of neural-related genes is compatible with stemness in solid cancers.Epigenetics & chromatin · 2023Article
- Oncogenic signaling-mediated regulation of chromatin during tumorigenesis.Cancer metastasis reviews · 2023Review
- Neural induction drives body axis formation during embryogenesis, but a neural induction-like process drives tumorigenesis in postnatal animals.Frontiers in cell and developmental biology · 2023Review
- Nerves in gastrointestinal cancer: from mechanism to modulations.Nature reviews. Gastroenterology & hepatology · 2022Review
- Neural is Fundamental: Neural Stemness as the Ground State of Cell Tumorigenicity and Differentiation Potential.Stem cell reviews and reports · 2022Review
- Coordinated regulation of the ribosome and proteasome by PRMT1 in the maintenance of neural stemness in cancer cells and neural stem cells.The Journal of biological chemistry · 2021Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Misexpression of chromatin modification factors and changed epigenetic modifications play crucial roles for tumorigenesis. Our previous studies demonstrated that inhibition of epigenetic modification enzymes EZH2, LSD1, DNMTs, and HDACs caused post-mitotic neuron-like differentiation in different cancer cells. However, how they regulate neuronal differentiation in cancer cells was unknown. Here, we show that EZH2, LSD1, DNMT1, and HDAC1 form interactions themselves, meanwhile, they also interact with SMAD proteins and β-CATENIN in cancer cells. Chemical inhibition of these enzymes leads to reduced level of proteins except HDAC1. The change in protein level and/or enzymatic activities further result in changed chromatin modifications on neuronal gene promoters, and activation of neuronal genes. Inhibition of these enzymes in neural progenitor cells (NPCs) also caused neuronal differentiation, similar to cancer cells. Particularly, EZH2 interacts with and required for the stability of LSD1, HDAC1, DNMT1, β-CATENIN, or SMAD2/4, via recruitment of deubiquitinase USP7. Reduced EZH2 leads to enhanced ubiquitination and degradation of these proteins, and decreased binding of LSD1, HDAC1, and DNMT1 to neuronal gene promoters, and lessened Wnt and TGFβ target gene activation. Hence, EZH2 sustains a series of proteins that promote tumorigenesis, in addition to its original function of histone methylation. Considering together with other studies, we conclude that these chromatin modification factors function in the same way in cancer cells as in neural progenitor/stem cells. The similarity between cancer cells and neural progenitor/stem cells provides an insight into the essence and unified framework for cancer initiation and progression, and are suggestive for novel strategies of cancer therapy.
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