ArticleJournal of hematology & oncology2018
The polycomb group protein EZH2 induces epithelial-mesenchymal transition and pluripotent phenotype of gastric cancer cells by binding to PTEN promoter.
Article in Journal of hematology & oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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Who cites it
76 citing papers in PubMed, 129 citations in OpenAlex.
- Ion chromatography-ultra-high-resolution mass spectrometry reveals EZH2-driven reprogramming of nucleic acid and protein methylation.Analytica chimica acta · 2026Article
- Exploring EZH2-Linked lncRNAs in Gastric Cancer: Insights from Sequencing Data and Gene Modulation.Biochemical genetics · 2026Article
- NRF1 predominantly causes EZH2 overexpression in cancer cells.Cell death & disease · 2026Article
- Histone modification-regulated LncRNA DLEU1 interacts with ASCC2/ALKBH3 complex to drive DNA repair, antioxidant homeostasis and glucose metabolism in gastric cancer.Biomarker research · 2026Article
- Review
- Construction of an Oxidative Stress Risk Model to Analyze the Correlation Between Liver Cancer and Tumor Immunity.Current cancer drug targets · 2025Article
- EZH2 deletion does not affect acinar regeneration but restricts progression to pancreatic cancer in mice.JCI insight · 2024Article
- Epigenetic and Immune Profile Characteristics in Sinonasal Undifferentiated Carcinoma.Cancer medicine · 2024Article
- A Multi-Omics Prognostic Model Capturing Tumor Stemness and the Immune Microenvironment in Clear Cell Renal Cell Carcinoma.Biomedicines · 2024Article
- Lack of basic rationale in epithelial-mesenchymal transition and its related concepts.Cell & bioscience · 2024Review
- EZH2 Expression in Head-and-Neck Squamous Cell Cancer in Young Patients.International journal of molecular sciences · 2024Article
- Discovery of a novel, highly potent EZH2 PROTAC degrader for targeting non-canonical oncogenic functions of EZH2.European journal of medicinal chemistry · 2024Article
- EZH2-interacting lncRNAs contribute to gastric tumorigenesis; a review on the mechanisms of action.Molecular biology reports · 2024Review
- Insight into the Inhibitory Mechanism of Embryonic Ectoderm Development Subunit by Triazolopyrimidine Derivatives as Inhibitors through Molecular Dynamics Simulation.Molecules (Basel, Switzerland) · 2023Article
- Article
- Tumor-suppressive functions of protein lysine methyltransferases.Experimental & molecular medicine · 2023Review
- EZH2-H3K27me3-mediated silencing of mir-139-5p inhibits cellular senescence in hepatocellular carcinoma by activating TOP2A.Journal of experimental & clinical cancer research : CR · 2023Article
- Nicardipine is a putative EED inhibitor and has high selectivity and potency against chemoresistant prostate cancer in preclinical models.British journal of cancer · 2023Article
- The clinicopathological and prognostic significances of EZH2 expression in urological cancers: A meta‑analysis and bioinformatics analysis.Oncology letters · 2023Article
- Comprehensive analysis of immune subtypes reveals the prognostic value of cytotoxicity and FAPCancer immunology, immunotherapy : CII · 2023Article
16 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe influences of oncogenic Ezh2 on the progression and prognosis of gastric cancer (GC) and the underlying mechanisms are still poorly understood. Here, we aimed at investigating clinicopathological significance of Ezh2 in GC and the mechanisms underlying its function in GC development.
methodsThe expression level of Ezh2 was determined by qRT-PCR, immunoblot, and immunohistochemistry analysis in 156 pairs of GC tissues and adjacent normal gastric mucosa tissues. The biological functions of Ezh2 were assessed by in vitro and in vivo functional experiments. Chromatin immunoprecipitation (ChIP), luciferase, and Western blotting analyses were utilized to identify the relationship between Ezh2 and the PTEN/Akt signaling.
resultsThe expression of Ezh2 was higher in gastric cancer tissues in comparison with para-nontumorous epithelium. High expression of Ezh2 was associated with more aggressive biological behavior and poor prognosis in GC. In vitro studies indicated that Ezh2 promoted GC cells' proliferation and clonogenicity. Besides, Ezh2 led to the acquisition of epithelial-mesenchymal transition (EMT) phenotype of GC cells and enhanced GC cell migration and invasion capacity. In particular, Ezh2 strengthened sphere-forming capacity of GC cells, indicating its role in the enrichment of GC stem cells. Furthermore, we found that PTEN/Akt signaling contributed to the effects of Ezh2 on cancer stem cells (CSC) and EMT phenotype in GC cells, and blocking PTEN signaling significantly rescued the effects of Ezh2.
conclusionsTaken together, Ezh2 has a central role in regulating diverse aspects of the pathogenesis of GC in part by involving PTEN/Akt signaling, indicating that it could be an independent prognostic factor and potential therapeutic target.
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