ArticleMolecular cancer research : MCR2013
NF-YA underlies EZH2 upregulation and is essential for proliferation of human epithelial ovarian cancer cells.
Article in Molecular cancer research : MCR, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 57 citations in OpenAlex.
- NFYA-mediated promotion of castration-resistant prostate cancer progression through EGR4 regulation.Discover oncology · 2024Article
- Article
- Live cell dynamics of the NF-Y transcription factor.Scientific reports · 2021Article
- A CCAAT-binding factor, SlNFYA10, negatively regulates ascorbate accumulation by modulating the D-mannose/L-galactose pathway in tomato.Horticulture research · 2020Article
- Review
- CREB acts as a common transcription factor for major epigenetic repressors; DNMT3B, EZH2, CUL4B and E2F6.Medical oncology (Northwood, London, England) · 2020Article
- CYP27B1 Downregulation: A New Molecular Mechanism Regulating EZH2 in Ovarian Cancer Tumorigenicity.Frontiers in cell and developmental biology · 2020Article
- Transcription factor NFYA promotes G1/S cell cycle transition and cell proliferation by transactivating cyclin D1 and CDK4 in clear cell renal cell carcinoma.American journal of cancer research · 2020Article
- Epigenetic role of the nuclear factor NF-Y on ID gene family in endometrial tissues of women with endometriosis: a case control study.Reproductive biology and endocrinology : RB&E · 2019Article
- Analysis of cyclin E co-expression genes reveals nuclear transcription factor Y subunit alpha is an oncogene in gastric cancer.Chronic diseases and translational medicine · 2019Article
- The Identification and Analysis of mRNA-lncRNA-miRNA Cliques From the Integrative Network of Ovarian Cancer.Frontiers in genetics · 2019Article
- MicroRNA-132 Plays an Independent Prognostic Role in Pancreatic Ductal Adenocarcinoma and Acts as a Tumor Suppressor.Technology in cancer research & treatment · 2019Article
- Emerging EZH2 Inhibitors and Their Application in Lymphoma.Current hematologic malignancy reports · 2018Review
- Protein kinase A-mediated phosphorylation regulates STAT3 activation and oncogenic EZH2 activity.Oncogene · 2018Article
- Histone Methyltransferase EZH2: A Therapeutic Target for Ovarian Cancer.Molecular cancer therapeutics · 2018Review
- LINC01016 promotes the malignant phenotype of endometrial cancer cells by regulating the miR-302a-3p/miR-3130-3p/NFYA/SATB1 axis.Cell death & disease · 2018Article
- Screening of potentially crucial genes and regulatory factors involved in epithelial ovarian cancer using microarray analysis.Oncology letters · 2017Article
- EZH2-mediated epigenetic silencing of TIMP2 promotes ovarian cancer migration and invasion.Scientific reports · 2017Article
- Histone demethylase KDM2B upregulates histone methyltransferase EZH2 expression and contributes to the progression of ovarian cancer in vitro and in vivo.OncoTargets and therapy · 2017Article
- Transcription factor NF‑YA promotes a malignant phenotype by upregulating fatty acid synthase expression.Molecular medicine reports · 2016Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Epithelial ovarian cancer (EOC) accounts for the most gynecologic malignancy-associated deaths in the United States. Enhancer of zeste homolog 2 (EZH2), which silences gene expression through generating trimethylation on lysine 27 residue of histone H3 (H3K27Me3), is often overexpressed in EOCs and has been suggested as a therapeutic target. However, the mechanism underlying EZH2 overexpression in EOCs is unknown. Here, we show that EZH2 is upregulated at the transcription level, and two CCAAT boxes in the proximal regions of the human EZH2 gene promoter are critical for its transcription in EOC cells. Indeed, NF-YA, the regulatory subunit of the CCAAT-binding transcription factor NF-Y, is expressed at higher levels in human EOCs than in primary human ovarian surface epithelial (HOSE) cells. In addition, there is a positive correlation between expression of NF-YA and EZH2 in EOCs. Notably, high NF-YA expression predicts shorter overall survival in patients with EOCs. The association of NF-YA with the promoter of the human EZH2 gene is enhanced in human EOC cells compared with primary HOSE cells. Significantly, knockdown of NF-YA downregulates EZH2, decreases H3K27Me3 levels, and suppresses the growth of human EOC cells both in vitro and in a xenograft mouse model. Notably, NF-YA knockdown induces apoptosis of EOC cells and ectopic EZH2 expression partially rescues apoptosis induced by NF-YA knockdown. Together, these data reveal that NF-Y is a key regulator of EZH2 expression and is required for EOC cell proliferation, thus representing a novel target for developing EOC therapeutics.
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Registered trials
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