ArticleCancers2021
Disruption of YY1-EZH2 Interaction Using Synthetic Peptides Inhibits Breast Cancer Development.
Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 36 citations in OpenAlex.
- Activation of EZH2 Promoter Is Mediated by MAPK Signaling Regulated Transcription Factors in Anaplastic Thyroid Cancer.International journal of molecular sciences · 2026Article
- Review
- Intrinsic mechanotransduction during apical constriction licenses lineage competence in pluripotent stem cells.bioRxiv : the preprint server for biology · 2025Article
- The YYR (YY1- RKIP) Regulatory Axis in the pathogenesis of Cancer and Immune Evasion.Journal of experimental & clinical cancer research : CR · 2025Review
- CircCDYL Association With hnRNPL Modulates CDYL Isoform Switching in Breast Cancer Cells.Cancer science · 2025Article
- EZH2 suppresses IR-induced ferroptosis by forming a co-repressor complex with HIF-1α to inhibit ACSL4: Targeting EZH2 enhances radiosensitivity in KDM6A-deficient esophageal squamous carcinoma.Cell death and differentiation · 2025Article
- LncRNA PTENP1/miR-21/PTEN Axis Modulates EMT and Drug Resistance in Cancer: Dynamic Boolean Modeling for Cell Fates in DNA Damage Response.International journal of molecular sciences · 2024Article
- Biological Activity of Natural and Synthetic Peptides as Anticancer Agents.International journal of molecular sciences · 2024Review
- Morphological Changes Induced by TKS4 Deficiency Can Be Reversed by EZH2 Inhibition in Colorectal Carcinoma Cells.Biomolecules · 2024Article
- EZH2-Myc Hallmark in Oncovirus/Cytomegalovirus Infections and Cytomegalovirus' Resemblance to Oncoviruses.Cells · 2024Review
- JMJD3 regulate H3K27me3 modification via interacting directly with TET1 to affect spermatogonia self-renewal and proliferation.BMC genomics · 2024Article
- Long non-coding RNAs PTENP1, GNG12-AS1, MAGI2-AS3 and MEG3 as tumor suppressors in breast cancer and their associations with clinicopathological parameters.Cancer biomarkers : section A of Disease markers · 2024Article
- Aquatic Peptide: The Potential Anti-Cancer and Anti-Microbial Activity of GE18 Derived from Pathogenic FungusMolecules (Basel, Switzerland) · 2023Article
- Review
- Article
- Targeting Transcription Factor YY1 for Cancer Treatment: Current Strategies and Future Directions.Cancers · 2023Review
- The roles of EZH2 in cancer and its inhibitors.Medical oncology (Northwood, London, England) · 2023Review
- siRNA and targeted delivery systems in breast cancer therapy.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Review
- RBM14 as a novel epigenetic-activated tumor oncogene is implicated in the reprogramming of glycolysis in lung cancer.World journal of surgical oncology · 2023Article
- Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Enhancer of zeste homolog 2 (EZH2) is a methyltransferase to mediate lysine 27 trimethylation in histone H3 (i.e., H3K27me3) and repress gene expression. In solid tumors, EZH2 promotes oncogenesis and is considered a therapeutic target. As a transcription factor, Yin Yang 1 (YY1) recruits EZH2 through its oncoprotein binding (OPB) domain to establish gene repression. In this study, we mapped the YY1 protein binding (YPB) domain on EZH2 to a region of 27 amino acids. Both YPB and OPB domain synthetic peptides could disrupt YY1EZH2 interaction, markedly reduce breast cancer cell viability, and efficiently inhibit tumor growth in a xenograft mouse model. We analyzed MDA-MB-231 cells treated with YPB, OPB, and control peptides by chromatin immunoprecipitation DNA sequencing (ChIP-seq) using an antibody against H3K27me3. YPB and OPB treatments altered H3K27me3 on 465 and 1137 genes, respectively, compared to the control. Of these genes, 145 overlapped between the two peptides. Among them, PTENP1, the PTEN pseudogene, showed reduced H3K27me3 signal when treated by either YPB or OPB peptide. Consistently, the two peptides enhanced both PTENP1 and PTEN expression with concomitantly reduced AKT activation. Further studies validated PTENP1's contribution to the anticancer activity of YPB and OPB peptides.
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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.