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miR-96-5p Suppresses the Progression of Nasopharyngeal Carcinoma by Targeting CDK1

BACKGROUND: Nasopharyngeal carcinoma (NPC) is a malignant tumor that occurs in the nasopharyngeal mucosa. Clinically, radiotherapy is the preferred treatment for NPC, and cervical lymph node metastasis is easy to emerge in the early stage. Therefore, this study aimed to investigate the role and pote...

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Autores principales: Luo, Xiaoqin, He, Xian, Liu, Xing, Zhong, Lunkun, Hu, Wenjian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7406360/
https://www.ncbi.nlm.nih.gov/pubmed/32801769
http://dx.doi.org/10.2147/OTT.S248338
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author Luo, Xiaoqin
He, Xian
Liu, Xing
Zhong, Lunkun
Hu, Wenjian
author_facet Luo, Xiaoqin
He, Xian
Liu, Xing
Zhong, Lunkun
Hu, Wenjian
author_sort Luo, Xiaoqin
collection PubMed
description BACKGROUND: Nasopharyngeal carcinoma (NPC) is a malignant tumor that occurs in the nasopharyngeal mucosa. Clinically, radiotherapy is the preferred treatment for NPC, and cervical lymph node metastasis is easy to emerge in the early stage. Therefore, this study aimed to investigate the role and potential molecular mechanisms of miR-96-5p in NPC cells to develop new therapeutic horizons. METHODS: The expression of miR-96-5p and CDK1 was measured by RT-qPCR or Western blot. The target relationship between miR-96-5p and CDK1 was confirmed by luciferase reporter assay. CCK-8, sphere formation, flow cytometry and colony formation assay were employed to examine cell viability, stem-like property, apoptosis and cycle, respectively. Male BALB/c nude mice model (6–8 weeks, weigh 18–20 g) was used to evaluate the effect of miR-96-5p on tumor growth in vivo. RESULTS: miR-96-5p was lowly expressed and CDK1 was highly expressed in NPC tissues and cell lines. CDK1 was identified as a direct target of miR-96-5p, and its expression was negatively regulated by miR-96-5p. By targeting CDK1, miR-96-5p overexpression significantly inhibited tumor sphere formation, promoted apoptosis and cell cycle arrest in CNE-2Z cells. Importantly, CCK-8 and colony formation assay demonstrated that elevated miR-96-5p enhanced the radiotherapy and chemotherapy sensitivity of CNE-2Z cells. Animal experiments showed that the overexpression of miR-96-5p reduced tumor weight and size in tumor-bearing mice and inhibited the expression of stem-like marker proteins and apoptosis-related proteins. CONCLUSION: These results, together, suggested that miR-96-5p induced cell cycle arrest and apoptosis, inhibited stem-like property, and enhanced the radiochemical sensitivity of NPC by targeting CDK1. In short, miR-96-5p may be a diagnostic and therapeutic target for NPC.
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spelling pubmed-74063602020-08-14 miR-96-5p Suppresses the Progression of Nasopharyngeal Carcinoma by Targeting CDK1 Luo, Xiaoqin He, Xian Liu, Xing Zhong, Lunkun Hu, Wenjian Onco Targets Ther Original Research BACKGROUND: Nasopharyngeal carcinoma (NPC) is a malignant tumor that occurs in the nasopharyngeal mucosa. Clinically, radiotherapy is the preferred treatment for NPC, and cervical lymph node metastasis is easy to emerge in the early stage. Therefore, this study aimed to investigate the role and potential molecular mechanisms of miR-96-5p in NPC cells to develop new therapeutic horizons. METHODS: The expression of miR-96-5p and CDK1 was measured by RT-qPCR or Western blot. The target relationship between miR-96-5p and CDK1 was confirmed by luciferase reporter assay. CCK-8, sphere formation, flow cytometry and colony formation assay were employed to examine cell viability, stem-like property, apoptosis and cycle, respectively. Male BALB/c nude mice model (6–8 weeks, weigh 18–20 g) was used to evaluate the effect of miR-96-5p on tumor growth in vivo. RESULTS: miR-96-5p was lowly expressed and CDK1 was highly expressed in NPC tissues and cell lines. CDK1 was identified as a direct target of miR-96-5p, and its expression was negatively regulated by miR-96-5p. By targeting CDK1, miR-96-5p overexpression significantly inhibited tumor sphere formation, promoted apoptosis and cell cycle arrest in CNE-2Z cells. Importantly, CCK-8 and colony formation assay demonstrated that elevated miR-96-5p enhanced the radiotherapy and chemotherapy sensitivity of CNE-2Z cells. Animal experiments showed that the overexpression of miR-96-5p reduced tumor weight and size in tumor-bearing mice and inhibited the expression of stem-like marker proteins and apoptosis-related proteins. CONCLUSION: These results, together, suggested that miR-96-5p induced cell cycle arrest and apoptosis, inhibited stem-like property, and enhanced the radiochemical sensitivity of NPC by targeting CDK1. In short, miR-96-5p may be a diagnostic and therapeutic target for NPC. Dove 2020-07-30 /pmc/articles/PMC7406360/ /pubmed/32801769 http://dx.doi.org/10.2147/OTT.S248338 Text en © 2020 Luo et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).
spellingShingle Original Research
Luo, Xiaoqin
He, Xian
Liu, Xing
Zhong, Lunkun
Hu, Wenjian
miR-96-5p Suppresses the Progression of Nasopharyngeal Carcinoma by Targeting CDK1
title miR-96-5p Suppresses the Progression of Nasopharyngeal Carcinoma by Targeting CDK1
title_full miR-96-5p Suppresses the Progression of Nasopharyngeal Carcinoma by Targeting CDK1
title_fullStr miR-96-5p Suppresses the Progression of Nasopharyngeal Carcinoma by Targeting CDK1
title_full_unstemmed miR-96-5p Suppresses the Progression of Nasopharyngeal Carcinoma by Targeting CDK1
title_short miR-96-5p Suppresses the Progression of Nasopharyngeal Carcinoma by Targeting CDK1
title_sort mir-96-5p suppresses the progression of nasopharyngeal carcinoma by targeting cdk1
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7406360/
https://www.ncbi.nlm.nih.gov/pubmed/32801769
http://dx.doi.org/10.2147/OTT.S248338
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