ArticleMolecular medicine reports2018
Combined analysis of gene expression and genome binding profiles identified potential therapeutic targets of ciclopirox in Ewing sarcoma.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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
5 citing papers in PubMed, 8 citations in OpenAlex.
- Repurposing of Ciclopirox to Overcome the Limitations of Zidovudine (Azidothymidine) against Multidrug-Resistant Gram-Negative Bacteria.Pharmaceutics · 2022Article
- Fosciclopirox suppresses growth of high-grade urothelial cancer by targeting the γ-secretase complex.Cell death & disease · 2021Article
- Reposition of the Fungicide Ciclopirox for Cancer Treatment.Recent patents on anti-cancer drug discovery · 2021Review
- Sugar and iron: Toward understanding the antibacterial effect of ciclopirox in Escherichia coli.PloS one · 2019Article
- Comparison of tumor related signaling pathways with known compounds to determine potential agents for lung adenocarcinoma.Thoracic cancer · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ciclopirox (CPX) is a synthetic antifungal drug that is mainly used to treat dermatomycoses. The aim of the present study was to determine whether CPX could influence Ewing sarcoma progression. The present study suggested that CPX treatment may inhibit Ewing sarcoma (ES) progression through Ewing sarcoma breakpoint region 1‑Friend leukemia integration 1 (EWS‑FLI1), a common fusion transcript structure in patients with ES. To determine the underlying mechanisms of ES progression, cross analysis was conducted on three high‑throughput genome or transcript me datasets from the Gene Expression Omnibus. The results indicated that CPX may inhibit ES growth by affecting vasculature development and DNA replication. A combination of genome‑wide expression and binding profiles revealed several potential targets for CPX in ES, including collagen type I α2 chain, N‑myc proto‑oncogene and transforming growth factor β1, which contained significantly enriched binding peaks of FLI1. In addition, network analysis, including a protein‑protein interaction network and a transcription regulatory network, provided further detailed information about the roles of CPX in ES. This study may provide a novel solution for ES treatment and may also aid in improving its prognosis.
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Registered trials
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