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Interferon regulatory factor 5-induced upregulation of zinc-finger protein 217 promotes pancreatic carcinoma progression

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. T...

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Autores principales: Qiao, Xiao, Lv, Shengxiang, Qiao, Yan, Wang, Fei, Miao, Lin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8985198/
https://www.ncbi.nlm.nih.gov/pubmed/35362545
http://dx.doi.org/10.3892/mmr.2022.12705
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author Qiao, Xiao
Lv, Shengxiang
Qiao, Yan
Wang, Fei
Miao, Lin
author_facet Qiao, Xiao
Lv, Shengxiang
Qiao, Yan
Wang, Fei
Miao, Lin
author_sort Qiao, Xiao
collection PubMed
description 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 in vitro. In conclusion, ZNF217 silencing exerted notable inhibitory effects on the progression of PC. Thus, ZNF217 may serve as a potential target for developing novel therapeutic strategies for PC.
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spelling pubmed-89851982022-04-08 Interferon regulatory factor 5-induced upregulation of zinc-finger protein 217 promotes pancreatic carcinoma progression Qiao, Xiao Lv, Shengxiang Qiao, Yan Wang, Fei Miao, Lin Mol Med Rep Articles 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 in vitro. In conclusion, ZNF217 silencing exerted notable inhibitory effects on the progression of PC. Thus, ZNF217 may serve as a potential target for developing novel therapeutic strategies for PC. D.A. Spandidos 2022-05 2022-03-30 /pmc/articles/PMC8985198/ /pubmed/35362545 http://dx.doi.org/10.3892/mmr.2022.12705 Text en Copyright: © Qiao et al. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Qiao, Xiao
Lv, Shengxiang
Qiao, Yan
Wang, Fei
Miao, Lin
Interferon regulatory factor 5-induced upregulation of zinc-finger protein 217 promotes pancreatic carcinoma progression
title Interferon regulatory factor 5-induced upregulation of zinc-finger protein 217 promotes pancreatic carcinoma progression
title_full Interferon regulatory factor 5-induced upregulation of zinc-finger protein 217 promotes pancreatic carcinoma progression
title_fullStr Interferon regulatory factor 5-induced upregulation of zinc-finger protein 217 promotes pancreatic carcinoma progression
title_full_unstemmed Interferon regulatory factor 5-induced upregulation of zinc-finger protein 217 promotes pancreatic carcinoma progression
title_short Interferon regulatory factor 5-induced upregulation of zinc-finger protein 217 promotes pancreatic carcinoma progression
title_sort interferon regulatory factor 5-induced upregulation of zinc-finger protein 217 promotes pancreatic carcinoma progression
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8985198/
https://www.ncbi.nlm.nih.gov/pubmed/35362545
http://dx.doi.org/10.3892/mmr.2022.12705
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