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EZH2 regulates oncomiR-200c and EMT markers in esophageal squamous cell carcinomas

EZH2, as a histone methyltransferase, has been associated with cancer development and metastasis possibly through the regulation of microRNAs and cellular pathways such as EMT. In this study, the effect of EZH2 expression on miR-200c and important genes of the EMT pathway was investigated in esophag...

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Autores principales: Nourmohammadi, Fatemeh, Forghanifard, Mohammad Mahdi, Abbaszadegan, Mohammad Reza, Zarrinpour, Vajiheh
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9622866/
https://www.ncbi.nlm.nih.gov/pubmed/36316365
http://dx.doi.org/10.1038/s41598-022-23253-2
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author Nourmohammadi, Fatemeh
Forghanifard, Mohammad Mahdi
Abbaszadegan, Mohammad Reza
Zarrinpour, Vajiheh
author_facet Nourmohammadi, Fatemeh
Forghanifard, Mohammad Mahdi
Abbaszadegan, Mohammad Reza
Zarrinpour, Vajiheh
author_sort Nourmohammadi, Fatemeh
collection PubMed
description EZH2, as a histone methyltransferase, has been associated with cancer development and metastasis possibly through the regulation of microRNAs and cellular pathways such as EMT. In this study, the effect of EZH2 expression on miR-200c and important genes of the EMT pathway was investigated in esophageal squamous cell carcinoma (ESCC). Comparative qRT-PCR was used to examine EZH2 expression in ESCC lines (YM-1 and KYSE‐30) following the separately transfected silencing and ectopic expressional EZH2 vectors in ESCC. Subsequently, expression of miR-200c and EMT markers was also assessed using qRT-PCR, western blotting and immunocytochemistry. Underexpression of Mir200c was detected in YM-1 and KYSE-30 cells after EZH2 silencing, while its overexpression was observed after EZH2 induced expression. Following EZH2 silencing, downregulation of mesenchymal markers and upregulation of epithelial markers were detected in the ESCCs. Our results demonstrate that EZH2 regulates the expression of miR-200c and critical EMT genes, implying that overexpression of Zeb2, Fibronectin, N-cadherin, and Vimentin lead to a mesenchymal phenotype and morphology while underexpression of epithelial genes, enhance cell migration after enforced expression of EZH2 in ESCCs. EZH2 gene can be a beneficial treatment marker for patients with esophageal cancer through decrease invasiveness of the disease and efficient response to neoadjuvant therapy.
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spelling pubmed-96228662022-11-02 EZH2 regulates oncomiR-200c and EMT markers in esophageal squamous cell carcinomas Nourmohammadi, Fatemeh Forghanifard, Mohammad Mahdi Abbaszadegan, Mohammad Reza Zarrinpour, Vajiheh Sci Rep Article EZH2, as a histone methyltransferase, has been associated with cancer development and metastasis possibly through the regulation of microRNAs and cellular pathways such as EMT. In this study, the effect of EZH2 expression on miR-200c and important genes of the EMT pathway was investigated in esophageal squamous cell carcinoma (ESCC). Comparative qRT-PCR was used to examine EZH2 expression in ESCC lines (YM-1 and KYSE‐30) following the separately transfected silencing and ectopic expressional EZH2 vectors in ESCC. Subsequently, expression of miR-200c and EMT markers was also assessed using qRT-PCR, western blotting and immunocytochemistry. Underexpression of Mir200c was detected in YM-1 and KYSE-30 cells after EZH2 silencing, while its overexpression was observed after EZH2 induced expression. Following EZH2 silencing, downregulation of mesenchymal markers and upregulation of epithelial markers were detected in the ESCCs. Our results demonstrate that EZH2 regulates the expression of miR-200c and critical EMT genes, implying that overexpression of Zeb2, Fibronectin, N-cadherin, and Vimentin lead to a mesenchymal phenotype and morphology while underexpression of epithelial genes, enhance cell migration after enforced expression of EZH2 in ESCCs. EZH2 gene can be a beneficial treatment marker for patients with esophageal cancer through decrease invasiveness of the disease and efficient response to neoadjuvant therapy. Nature Publishing Group UK 2022-10-31 /pmc/articles/PMC9622866/ /pubmed/36316365 http://dx.doi.org/10.1038/s41598-022-23253-2 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Nourmohammadi, Fatemeh
Forghanifard, Mohammad Mahdi
Abbaszadegan, Mohammad Reza
Zarrinpour, Vajiheh
EZH2 regulates oncomiR-200c and EMT markers in esophageal squamous cell carcinomas
title EZH2 regulates oncomiR-200c and EMT markers in esophageal squamous cell carcinomas
title_full EZH2 regulates oncomiR-200c and EMT markers in esophageal squamous cell carcinomas
title_fullStr EZH2 regulates oncomiR-200c and EMT markers in esophageal squamous cell carcinomas
title_full_unstemmed EZH2 regulates oncomiR-200c and EMT markers in esophageal squamous cell carcinomas
title_short EZH2 regulates oncomiR-200c and EMT markers in esophageal squamous cell carcinomas
title_sort ezh2 regulates oncomir-200c and emt markers in esophageal squamous cell carcinomas
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9622866/
https://www.ncbi.nlm.nih.gov/pubmed/36316365
http://dx.doi.org/10.1038/s41598-022-23253-2
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