ArticleEpigenetics2015
Prolonged re-expression of the hypermethylated gene EPB41L3 using artificial transcription factors and epigenetic drugs.
Article in Epigenetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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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.
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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
14 citing papers in PubMed, 30 citations in OpenAlex.
- TET2: a critical regulatory hub with broad therapeutic implications across human diseases.Frontiers in immunology · 2026Review
- Expression and hypermethylation of JAM and EPB41L3 in cervical squamous cell carcinoma: Clinical significance and applications.Histology and histopathology · 2024Article
- Review
- Review
- Epigenetic Editing in Prostate Cancer: Challenges and Opportunities.Epigenetics · 2022Review
- Bioethical issues in genome editing by CRISPR-Cas9 technology.Turkish journal of biology = Turk biyoloji dergisi · 2020Article
- RNA Biology Provides New Therapeutic Targets for Human Disease.Frontiers in genetics · 2019Review
- Designer epigenome modifiers enable robust and sustained gene silencing in clinically relevant human cells.Nucleic acids research · 2018Article
- ZFP226 is a novel artificial transcription factor for selective activation of tumor suppressor KIBRA.Scientific reports · 2018Article
- Host-cell DNA methylation patterns during high-risk HPV-induced carcinogenesis reveal a heterogeneous nature of cervical pre-cancer.Epigenetics · 2018Article
- Waking up dormant tumor suppressor genes with zinc fingers, TALEs and the CRISPR/dCas9 system.Oncotarget · 2016Article
- Writing of H3K4Me3 overcomes epigenetic silencing in a sustained but context-dependent manner.Nature communications · 2016Article
- Re-expression of Selected Epigenetically Silenced Candidate Tumor Suppressor Genes in Cervical Cancer by TET2-directed Demethylation.Molecular therapy : the journal of the American Society of Gene Therapy · 2016Article
- Epigenetic Editing: On the Verge of Reprogramming Gene Expression at Will.Current genetic medicine reports · 2016Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epigenetic silencing of tumor suppressor genes (TSGs) is considered a significant event in the progression of cancer. For example, EPB41L3, a potential biomarker in cervical cancer, is often silenced by cancer-specific promoter methylation. Artificial transcription factors (ATFs) are unique tools to re-express such silenced TSGs to functional levels; however, the induced effects are considered transient. Here, we aimed to improve the efficiency and sustainability of gene re-expression using engineered zinc fingers fused to VP64 (ZF-ATFs) or DNA methylation modifiers (ZF-Tet2 or ZF-TDG) and/or by co-treatment with epigenetic drugs [5-aza-2'-deoxycytidine or Trichostatin A (TSA)]. The EPB41L3-ZF effectively bound its methylated endogenous locus, as also confirmed by ChIP-seq. ZF-ATFs reactivated the epigenetically silenced target gene EPB41L3 (∼ 10-fold) in breast, ovarian, and cervical cancer cell lines. Prolonged high levels of EPB41L3 (∼ 150-fold) induction could be achieved by short-term co-treatment with epigenetic drugs. Interestingly, for otherwise ineffective ZF-Tet2 or ZF-TDG treatments, TSA facilitated re-expression of EPB41L3 up to twofold. ATF-mediated re-expression demonstrated a tumor suppressive role for EPB41L3 in cervical cancer cell lines. In conclusion, epigenetic reprogramming provides a novel way to improve sustainability of re-expression of epigenetically silenced promoters.
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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.