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miR-186 regulates epithelial–mesenchymal transformation to promote nasopharyngeal carcinoma metastasis by targeting ZEB1()

OBJECTIVES: Nasopharyngeal carcinoma (NPC) is an aggressive epithelial cancer. The expression of miR-186 is decreased in a variety of malignancies and can promote the invasion and metastasis of cancer cells. This study aimed to explore the role and possible mechanism of miR-186 in the metastasis and...

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Autores principales: Tang, Liangke, Xiang, Yalang, Zhou, Jing, Li, Tao, Jia, Tingting, Du, Guobo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10679499/
https://www.ncbi.nlm.nih.gov/pubmed/37989078
http://dx.doi.org/10.1016/j.bjorl.2023.101358
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author Tang, Liangke
Xiang, Yalang
Zhou, Jing
Li, Tao
Jia, Tingting
Du, Guobo
author_facet Tang, Liangke
Xiang, Yalang
Zhou, Jing
Li, Tao
Jia, Tingting
Du, Guobo
author_sort Tang, Liangke
collection PubMed
description OBJECTIVES: Nasopharyngeal carcinoma (NPC) is an aggressive epithelial cancer. The expression of miR-186 is decreased in a variety of malignancies and can promote the invasion and metastasis of cancer cells. This study aimed to explore the role and possible mechanism of miR-186 in the metastasis and epithelial–mesenchymal transformation (EMT) of NPC. METHODS: The expression of miR-186 in NPC tissues and cells was detected by RT-PCR. Then, miR-186 mimic was used to transfect NPC cell lines C666-1 and CNE-2, and cell activity, invasion and migration were detected by CCK8, transwell and scratch assay, respectively. The expression of EMT-related proteins was analyzed by western blotting analysis. The binding relationship between miR-186 and target gene Zinc Finger E-Box Binding Homeobox 1 (ZEB1) was confirmed by double luciferase assay. RESULTS: The expression of miR-186 in NPC was significantly decreased, and transfection of miR-186 mimic could significantly inhibit the cell activity, invasion, and migration, and regulate the protein expressions of E-cadherin, N-cadherin and vimentin in C666-1 and CNE-2 cells. Further experiments confirmed that miR-186 could directly target ZEB1 and negatively regulate its expression. In addition, ZEB1 has been confirmed to be highly expressed in NPC, and inhibition of ZEB1 could inhibit the activity, invasion, metastasis and EMT of NPC cells. And co-transfection of miR-186 mimic and si-ZEB1 could further inhibit the proliferation and metastasis of NPC. CONCLUSION: miR-186 may inhibit the proliferation, metastasis and EMT of NPC by targeting ZEB1, and the miR-186/ZEB1 axis plays an important role in NPC.
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spelling pubmed-106794992023-11-06 miR-186 regulates epithelial–mesenchymal transformation to promote nasopharyngeal carcinoma metastasis by targeting ZEB1() Tang, Liangke Xiang, Yalang Zhou, Jing Li, Tao Jia, Tingting Du, Guobo Braz J Otorhinolaryngol Original Article OBJECTIVES: Nasopharyngeal carcinoma (NPC) is an aggressive epithelial cancer. The expression of miR-186 is decreased in a variety of malignancies and can promote the invasion and metastasis of cancer cells. This study aimed to explore the role and possible mechanism of miR-186 in the metastasis and epithelial–mesenchymal transformation (EMT) of NPC. METHODS: The expression of miR-186 in NPC tissues and cells was detected by RT-PCR. Then, miR-186 mimic was used to transfect NPC cell lines C666-1 and CNE-2, and cell activity, invasion and migration were detected by CCK8, transwell and scratch assay, respectively. The expression of EMT-related proteins was analyzed by western blotting analysis. The binding relationship between miR-186 and target gene Zinc Finger E-Box Binding Homeobox 1 (ZEB1) was confirmed by double luciferase assay. RESULTS: The expression of miR-186 in NPC was significantly decreased, and transfection of miR-186 mimic could significantly inhibit the cell activity, invasion, and migration, and regulate the protein expressions of E-cadherin, N-cadherin and vimentin in C666-1 and CNE-2 cells. Further experiments confirmed that miR-186 could directly target ZEB1 and negatively regulate its expression. In addition, ZEB1 has been confirmed to be highly expressed in NPC, and inhibition of ZEB1 could inhibit the activity, invasion, metastasis and EMT of NPC cells. And co-transfection of miR-186 mimic and si-ZEB1 could further inhibit the proliferation and metastasis of NPC. CONCLUSION: miR-186 may inhibit the proliferation, metastasis and EMT of NPC by targeting ZEB1, and the miR-186/ZEB1 axis plays an important role in NPC. Elsevier 2023-11-06 /pmc/articles/PMC10679499/ /pubmed/37989078 http://dx.doi.org/10.1016/j.bjorl.2023.101358 Text en © 2023 Associação Brasileira de Otorrinolaringologia e Cirurgia Cérvico-Facial. Published by Elsevier España, S.L.U. https://creativecommons.org/licenses/by/4.0/This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Original Article
Tang, Liangke
Xiang, Yalang
Zhou, Jing
Li, Tao
Jia, Tingting
Du, Guobo
miR-186 regulates epithelial–mesenchymal transformation to promote nasopharyngeal carcinoma metastasis by targeting ZEB1()
title miR-186 regulates epithelial–mesenchymal transformation to promote nasopharyngeal carcinoma metastasis by targeting ZEB1()
title_full miR-186 regulates epithelial–mesenchymal transformation to promote nasopharyngeal carcinoma metastasis by targeting ZEB1()
title_fullStr miR-186 regulates epithelial–mesenchymal transformation to promote nasopharyngeal carcinoma metastasis by targeting ZEB1()
title_full_unstemmed miR-186 regulates epithelial–mesenchymal transformation to promote nasopharyngeal carcinoma metastasis by targeting ZEB1()
title_short miR-186 regulates epithelial–mesenchymal transformation to promote nasopharyngeal carcinoma metastasis by targeting ZEB1()
title_sort mir-186 regulates epithelial–mesenchymal transformation to promote nasopharyngeal carcinoma metastasis by targeting zeb1()
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10679499/
https://www.ncbi.nlm.nih.gov/pubmed/37989078
http://dx.doi.org/10.1016/j.bjorl.2023.101358
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