ArticleMolecular medicine reports2022
Interferon regulatory factor 5‑induced upregulation of zinc‑finger protein 217 promotes pancreatic carcinoma progression.
Article in Molecular medicine reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- Disruption of the novel nested geneeLife · 2025Article
- CRISPR screening reveals ZNF217 as a vulnerability in high-risk B-cell acute lymphoblastic leukemia.Theranostics · 2025Article
- Role of interferon regulatory factor 5 (IRF5) in tumor progression: Prognostic and therapeutic potential.Biochimica et biophysica acta. Reviews on cancer · 2024Review
- ZNF217: An Oncogenic Transcription Factor and Potential Therapeutic Target for Multiple Human Cancers.Cancer management and research · 2024Review
- The Intricate Interplay between the ZNF217 Oncogene and Epigenetic Processes Shapes Tumor Progression.Cancers · 2022Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to investigate the molecular mechanisms of zinc‑finger protein 217 (ZNF217) in pancreatic carcinoma (PC) progression. ZNF217‑associated expression and survival data from patients with PC were retrieved from the Gene Expression Profiling Interactive Analysis server. The mRNA expression level of ZNF217 was detected by reverse transcription‑quantitative PCR. Cell Counting Kit‑8, colony formation, wound‑healing and Transwell assays were conducted to assess cellular proliferation, migratory and invasive abilities. Proliferation was also examined by immunofluorescence detection of Ki67 expression, and chromatin immunoprecipitation (ChIP) and luciferase reporter assays were performed to detect the interaction between ZNF217 and interferon regulatory factor 5 (IRF5). ZNF217 was found to be significantly upregulated in tumor tissues and cancer cell lines, which was associated with a poor survival rate in patients with PC. ZNF217 silencing markedly suppressed cellular proliferation and migratory and invasive abilities, as well as decreased the expression of Ki67. IRF5 was also upregulated in PC tumor tissues and was shown to positively regulate the activity of the ZNF217 promoter and its mRNA expression levels. Furthermore, ChIP assays demonstrated that IRF5 bound to the promoter region of ZNF217
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