ArticleProceedings of the National Academy of Sciences of the United States of America2021
ZMYND8 preferentially binds phosphorylated EZH2 to promote a PRC2-dependent to -independent function switch in hypoxia-inducible factor-activated cancer.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 31 citations in OpenAlex.
- SPOP-mediated ZMYND8 ubiquitination and phase separation exclusion drives mTOR inhibitor resistance in kidney cancer.Nature communications · 2026Article
- Trophoblast cells rewire the epigenetic landscape of vascular smooth muscle cells to modulate plasticity: a regulatory axis disrupted in intrauterine growth restriction.Cell communication and signaling : CCS · 2026Article
- ZMYND8 promotes the Warburg effect and tumorigenesis through c-Myc activation in pancreatic cancer.Oncogene · 2025Article
- RACK7 Interacts with PRC2 Complex to Regulate Astrocyte Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- ZMYND8 drives HER2 antibody resistance in breast cancer via lipid control of IL-27.Nature communications · 2025Article
- HOXC-AS1 and EZH2 interaction increase HOXC9 expression and promote the malignant transformation of oral leukoplakia.Journal of Cancer · 2025Article
- Hypoxia makes EZH2 inhibitor not easy-advances of crosstalk between HIF and EZH2.Life metabolism · 2024Article
- Cell surface CD55 traffics to the nucleus leading to cisplatin resistance and stemness by inducing PRC2 and H3K27 trimethylation on chromatin in ovarian cancer.Molecular cancer · 2024Article
- ZMYND8 protects breast cancer stem cells against oxidative stress and ferroptosis through activation of NRF2.The Journal of clinical investigation · 2024Article
- TGFβ1-RCN3-TGFBR1 loop facilitates pulmonary fibrosis by orchestrating fibroblast activation.Respiratory research · 2023Article
- Hypoxia-mediated promotion of glucose metabolism in non-small cell lung cancer correlates with activation of the EZH2/FBXL7/PFKFB4 axis.Cell death & disease · 2023Article
- Zinc Finger MYND-Type Containing 8 (ZMYND8) Is Epigenetically Regulated in Mutant Isocitrate Dehydrogenase 1 (IDH1) Glioma to Promote Radioresistance.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- Identification of a NACC1-Regulated Gene Signature Implicated in the Features of Triple-Negative Breast Cancer.Biomedicines · 2023Article
- ZMYND8 is a master regulator of 27-hydroxycholesterol that promotes tumorigenicity of breast cancer stem cells.Science advances · 2022Article
- Targeting Triple-Negative Breast Cancer by a Novel Proteolysis Targeting Chimera Degrader of Enhancer of Zeste Homolog 2.ACS pharmacology & translational science · 2022Article
- Synthetic lethality of cyclin-dependent kinase inhibitor Dinaciclib withCell cycle (Georgetown, Tex.) · 2022Article
- Functional Roles of Bromodomain Proteins in Cancer.Cancers · 2021Review
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Both gene repressor (Polycomb-dependent) and activator (Polycomb-independent) functions of the Polycomb protein enhancer of zeste homolog 2 (EZH2) are implicated in cancer progression. EZH2 protein can be phosphorylated at various residues, such as threonine 487 (T487), by CDK1 kinase, and such phosphorylation acts as a Polycomb repressive complex 2 (PRC2) suppression "code" to mediate the gene repressor-to-activator switch of EZH2 functions. Here we demonstrate that the histone reader protein ZMYND8 is overexpressed in human clear cell renal cell carcinoma (ccRCC). ZMYND8 binds to EZH2, and their interaction is largely enhanced by CDK1 phosphorylation of EZH2 at T487. ZMYND8 depletion not only enhances Polycomb-dependent function of EZH2 in hypoxia-exposed breast cancer cells or von Hippel-Lindau (VHL)-deficient ccRCC cells, but also suppresses the FOXM1 transcription program. We further show that ZMYND8 is required for EZH2-FOXM1 interaction and is important for FOXM1-dependent matrix metalloproteinase (
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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.