ArticlePloS one2010
Epigenetic drugs can stimulate metastasis through enhanced expression of the pro-metastatic Ezrin gene.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 53 citations in OpenAlex.
- Targeting one-carbon metabolic vulnerabilities of metastasis with therapeutic potential.bioRxiv : the preprint server for biology · 2026Article
- Article
- Review
- PTEN phosphatase inhibits metastasis by negatively regulating the Entpd5/IGF1R pathway through ATF6.iScience · 2023Article
- Epidrugs: novel epigenetic regulators that open a new window for targeting osteoblast differentiation.Stem cell research & therapy · 2020Review
- H3K27 trimethylation and H3K9 dimethylation as poor prognostic markers for patients with esophageal squamous cell carcinoma.International journal of clinical and experimental pathology · 2019Article
- Ezrin mediates both HGF/Met autocrine and non-autocrine signaling-induced metastasis in melanoma.International journal of cancer · 2018Article
- Article
- The interaction of lncRNA EZR-AS1 with SMYD3 maintains overexpression of EZR in ESCC cells.Nucleic acids research · 2018Article
- Epigenetic Approaches to the Treatment of Dental Pulp Inflammation and Repair: Opportunities and Obstacles.Frontiers in genetics · 2018Review
- Detecting the location and significance of Ezrin protein expression in hepatocellular carcinoma.International journal of clinical and experimental pathology · 2018Article
- Histone H3 Acetyl K9 and Histone H3 Tri Methyl K4 as Prognostic Markers for Patients with Cervical Cancer.International journal of molecular sciences · 2017Article
- The role of REST and HDAC2 in epigenetic dysregulation of Nav1.5 and nNav1.5 expression in breast cancer.Cancer cell international · 2017Article
- Probing for a deeper understanding of rhabdomyosarcoma: insights from complementary model systems.Nature reviews. Cancer · 2015Review
- DNA demethylation and invasive cancer: implications for therapeutics.British journal of pharmacology · 2015Review
- CHST11 gene expression and DNA methylation in breast cancer.International journal of oncology · 2015Article
- Functional Role of G9a Histone Methyltransferase in Cancer.Frontiers in immunology · 2015Review
- Epigenome engineering in cancer: fairytale or a realistic path to the clinic?Frontiers in oncology · 2015Review
- Article
- Current and upcoming approaches to exploit the reversibility of epigenetic mutations in breast cancer.Breast cancer research : BCR · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Ezrin has been reported to be upregulated in many tumors and to participate in metastatic progression. No study has addressed epigenetic modification in the regulation of Ezrin gene expression, the importance of which is unknown. Here, we report that highly metastatic rhabdomyosarcoma (RMS) cells with high levels of Ezrin have elevated acetyl-H3-K9 and tri-methyl-H3-K4 as well as reduced DNA methylation at the Ezrin gene promoter. Conversely, poorly metastatic RMS cells with low levels of Ezrin have reduced acetyl-H3-K9 and elevated methylation. Thus epigenetic covalent modifications to histones within nucleosomes of the Ezrin gene promoter are linked to Ezrin expression, which in fact can be regulated by epigenetic mechanisms. Notably, treatment with histone deacetylase (HDAC) inhibitors or DNA demethylating agents could restore Ezrin expression and stimulate the metastatic potential of poorly metastatic RMS cells characterized by low Ezrin levels. However, the ability of epigenetic drugs to stimulate metastasis in RMS cells was inhibited by expression of an Ezrin-specific shRNA. Our data demonstrate the potential risk associated with clinical application of broadly acting covalent epigenetic modifiers, and highlight the value of combination therapies that include agents specifically targeting potent pro-metastatic genes.
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.