Evidence map›Paper›PMID 39437453›Full record

ArticleEuropean journal of cell biology2024

dCas9-HDAC8-EGFP fusion enables epigenetic editing of breast cancer cells by H3K9 deacetylation.

Mohammad Mijanur Rahman, Trygve O Tollefsbol

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in European journal of cell biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Review
  2. Review
  3. Gene Therapy Techniques and Delivery Methods (Review).Sovremennye tekhnologii v meditsine · 2025
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Mohammad Mijanur RahmanDepartment of Biology, University of Alabama at Birmingham, 902 14th Street South, Birmingham, AL 35294, USA.
Trygve O TollefsbolDepartment of Biology, University of Alabama at Birmingham, 902 14th Street South, Birmingham, AL 35294, USA; Comprehensive Cancer Center, University of Alabama at Birmingham, 1802 6th Avenue South, Birmingham, AL 35294, USA; Integrative Center for Aging Research, University of Alabama at Birmingham, Birmingham, AL, USA; Nutrition Obesity Research Center, University of Alabama at Birmingham, 1675 University Blvd, Birmingham, AL 35294, USA; Comprehensive Diabetes Center, University of Alabama at Birmingham, 1825 University Blvd, Birmingham, AL 35294, USA. Electronic address: trygve@uab.edu.

Funding

Combinatorial epigenetic-based prevention of breast cancerR01CA178441 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI TOLLEFSBOL, TRYGVE O · 2014 to 2025
$3.2M
Early life prevention of breast cancer with combined epigenetic botanicalsR01CA204346 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI TOLLEFSBOL, TRYGVE O · 2017 to 2021
$1.7M
NCI NIH HHS R01 CA178441NCI NIH HHS R01 CA204346
6 · The paper itself

Abstract

Epigenetic editing is thriving as a robust tool for manipulating transcriptional regulation and cell fate. Despite its regulatory role in gene downregulation, epigenetic editing with histone deacetylation has been sparsely studied, especially in the context of cancer. In this current study, we have reconstructed a dCas9-HDAC8-EGFP fusion to perform histone deacetylation on the promoter of the ESR1, TERT and CDKN1C genes for the first time in breast cancer cell lines MCF-7 and MDA-MB-231 as well as in HEK293T cells. Our results demonstrated that dCas9-HDAC8-EGFP in combination with appropriate gRNAs were able to downregulate the expression of the ESR1, TERT and CDKN1C genes transcriptionally by specifically depleting the H3K9ac level on the recruitment loci. The addition of histone deacetylase inhibitors was found to neutralize the outcomes of dCas9-HDAC8-EGFP-induced epigenetic editing. Furthermore, we observed a significant downregulation of full length ERα expression in epigenetically edited MCF-7 cells with consequential alteration in cellular response toward estradiol and tamoxifen treatment due to dCas9-HDAC8-EGFP mediated epigenetic editing of the ESR1 gene. Overall, dCas9-HDAC8-EGFP is a novel circuit that enabled downregulation of crucial genes with cellular outcome in breast cancer cells by preferentially inducing H3K9 deacetylation of specific promoter regions.

Indexed as

Breast NeoplasmsEpigenesis, GeneticGreen Fluorescent ProteinsHistone DeacetylasesHistonesAcetylationCRISPR-Associated Protein 9Estrogen Receptor alphaFemaleGene EditingHEK293 CellsHistone Deacetylase InhibitorsHumansMCF-7 CellsCRISPR-Associated Protein 9enhanced green fluorescent proteinEstrogen Receptor alphaGreen Fluorescent ProteinsHistone Deacetylase InhibitorsHistone DeacetylasesHistonesDCas9-HDAC8-EGFPEpigenetic editingHDAC inhibitorHistone deacetylation

Identifiers

PMID39437453
PMCPMC11677611

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Registered trials

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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.