ArticleNucleus (Austin, Tex.)2016
Identification of chromatin accessibility domains in human breast cancer stem cells.
Article in Nucleus (Austin, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- The Redox-Adhesion-Exosome (RAX) Hub in Cancer: Lipid Peroxidation-Driven EMT Plasticity and Ferroptosis Defense with HNE/MDA Signaling and Lipidomic Perspectives.Antioxidants (Basel, Switzerland) · 2025Review
- Synthetic Epigenetic Reprogramming of Mesenchymal to Epithelial States Using the CRISPR/dCas9 Platform in Triple Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- EMT Features in Claudin-Low versus Claudin-Non-Suppressed Breast Cancers and the Role of Epigenetic Modifications.Current issues in molecular biology · 2023Article
- Low HER2 expression in normal breast epithelium enables dedifferentiation and malignant transformation via chromatin opening.Disease models & mechanisms · 2023Article
- RhoC in association with TET2/WDR5 regulates cancer stem cells by epigenetically modifying the expression of pluripotency genes.Cellular and molecular life sciences : CMLS · 2022Article
- Distinct cytosine modification profiles define epithelial-to-mesenchymal cell-state transitions.Epigenomics · 2022Article
- Cooperative interaction between ERα and the EMT-inducer ZEB1 reprograms breast cancer cells for bone metastasis.Nature communications · 2022Article
- Article
- Sclerosing Sialadenitis Is Associated With Salivary Gland Hypofunction and a Unique Gene Expression Profile in Sjögren's Syndrome.Frontiers in immunology · 2021Article
- Novel mechanistic targets of forkhead box Q1 transcription factor in human breast cancer cells.Molecular carcinogenesis · 2020Article
- FOXN2 is downregulated in breast cancer and regulates migration, invasion, and epithelial- mesenchymal transition through regulation of SLUG.Cancer management and research · 2019Article
- LSD1 activation promotes inducible EMT programs and modulates the tumour microenvironment in breast cancer.Scientific reports · 2018Article
- Nucleolin modulates compartmentalization and dynamics of histone 2B-ECFP in the nucleolus.Nucleus (Austin, Tex.) · 2018Article
- Core signaling pathways in ovarian cancer stem cell revealed by integrative analysis of multi-marker genomics data.PloS one · 2018Article
- Priming of transcriptional memory responses via the chromatin accessibility landscape in T cells.Scientific reports · 2017Article
- Iterative Fragmentation Improves the Detection of ChIP-seq Peaks for Inactive Histone Marks.Bioinformatics and biology insights · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-to-mesenchymal transition (EMT) is physiological in embryogenesis and wound healing but also associated with the formation of cancer stem cells (CSCs). Many EMT signaling pathways are implicated in CSC formation, but the precise underlying mechanisms of CSC formation remain elusive. We have previously demonstrated that PKC is critical for EMT induction and CSC formation in inducible breast EMT/CSC models. Here, we used formaldehyde-assisted isolation of regulatory elements-sequencing (FAIRE-seq) to investigate DNA accessibility changes after PKC activation and determine how they influence EMT and CSC formation. During EMT, DNA accessibility principally increased in regions distant from transcription start sites, low in CpG content, and enriched with chromatin enhancer marks. ChIP-sequencing revealed that a subset of these regions changed from poised to active enhancers upon stimulation, with some even more acteylated in CSCs. While regions with increased accessibility were enriched for FOX, AP-1, TEAD, and TFAP2 motifs, those containing FOX and AP-1 motif were associated with increased expression of CSC-associated genes, while those with TFAP2 were associated with genes with increased expression in non-CSCs. Silencing of 2 members of the FOX family, FOXN2 and FOXQ1, repressed CSCs and the mesenchymal phenotype and inhibited the CSC gene signature. These novel, PKC-induced DNA accessibility regions help explain how the epigenomic plasticity of cells undergoing EMT leads to CSC gene activation.
Indexed as
Identifiers
What OpenQuestion holds
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.