ArticleBritish journal of cancer2019
EZH2 cooperates with E2F1 to stimulate expression of genes involved in adrenocortical carcinoma aggressiveness.
Article in British journal of cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- Noncanonical EZH2 activity cooperates with FOXM1 to drive tumorigenesis and advanced progression in HCC.Clinical and molecular hepatology · 2026Article
- Deciphering the Effect of Methyl 4‑Hydroxybenzoate on Breast Cancer by Bioinformatics and Experiments.ACS omega · 2026Article
- Noncanonical association of EZH2 with E2F1 promotes tumor proliferation through chromatin remodeling.Experimental & molecular medicine · 2025Article
- MOGEDN: small-sample cancer subtype classification with encoder-decoder networks for missing-omics recovery and biomarker discovery.Briefings in bioinformatics · 2025Article
- A targetable antioxidant defense mechanism to EZH2 inhibitors enhances tumor cell vulnerability to ferroptosis.Cell death & disease · 2025Article
- Apolipoprotein C1 and apoprotein E as potential therapeutic and prognostic targets for adrenocortical carcinoma.Cancer biomarkers : section A of Disease markers · 2025Article
- Developing a prognostic stratification model based on glutathione metabolism in thyroid cancer and validating RRM2's tumor-promoting role.Frontiers in oncology · 2025Article
- Enzyme-independent role of EZH2 in regulating cell cycle progression via the SKP2-KIP/CIP pathway.Scientific reports · 2024Article
- A comprehensive analysis of ribonucleotide reductase subunit M2 for carcinogenesis in pan-cancer.PloS one · 2024Article
- Advances in translational research of the rare cancer type adrenocortical carcinoma.Nature reviews. Cancer · 2023Review
- Age-related Changes in the Adrenal Cortex: Insights and Implications.Journal of the Endocrine Society · 2023Review
- β-Catenin-Driven Differentiation Is a Tissue-Specific Epigenetic Vulnerability in Adrenal Cancer.Cancer research · 2023Article
- Resistance to BRAF Inhibitors: EZH2 and Its Downstream Targets as Potential Therapeutic Options in Melanoma.International journal of molecular sciences · 2023Article
- Sevoflurane Offers Neuroprotection in a Cerebral Ischemia/Reperfusion Injury Rat Model Through the E2F1/EZH2/TIMP2 Regulatory Axis.Molecular neurobiology · 2022Article
- Methylation-dependent and -independent roles of EZH2 synergize in CDCA8 activation in prostate cancer.Oncogene · 2022Article
- PCLAF promotes neuroblastoma G1/S cell cycle progression via the E2F1/PTTG1 axis.Cell death & disease · 2022Article
- EZH2: Its regulation and roles in immune disturbance of SLE.Frontiers in pharmacology · 2022Review
- Screening and Validation of Significant Genes with Poor Prognosis in Pathologic Stage-I Lung Adenocarcinoma.Journal of oncology · 2022Article
- Targeting EZH2-mediated methylation of histone 3 inhibits proliferation of pediatric acute monocytic leukemia cellsCancer biology & therapy · 2021Article
- The noncanonical role of EZH2 in cancer.Cancer science · 2021Review
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEZH2 is overexpressed and associated with poor prognosis in adrenocortical carcinoma (ACC) and its inhibition reduces growth and aggressiveness of ACC cells in culture. Although EZH2 was identified as the methyltransferase that deposits the repressive H3K27me3 histone mark, it can cooperate with transcription factors to stimulate gene transcription.
methodsWe used bioinformatics approaches on gene expression data from three cohorts of patients and a mouse model of EZH2 ablation, to identify targets and mode of action of EZH2 in ACC. This was followed by ChIP and functional assays to evaluate contribution of identified targets to ACC pathogenesis.
resultsWe show that EZH2 mostly works as a transcriptional inducer in ACC, through cooperation with the transcription factor E2F1 and identify three positive targets involved in cell cycle regulation and mitosis i.e., RRM2, PTTG1 and ASE1/PRC1. Overexpression of these genes is associated with poor prognosis, suggesting a potential role in acquisition of aggressive ACC features. Pharmacological and siRNA-mediated inhibition of RRM2 blocks cell proliferation, induces apoptosis and inhibits cell migration, suggesting that it may be an interesting target in ACC.
conclusionsAltogether, these data show an unexpected role of EZH2 and E2F1 in stimulating expression of genes associated with ACC aggressiveness.
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