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MicroRNA-30a regulates cell proliferation, migration, invasion and apoptosis in human nasopharyngeal carcinoma via targeted regulation of ZEB2

MicroRNA-30a (miR-30a) was previously reported to serve as a tumor suppressor able to inhibit the development and progression of certain types of cancer. A number of previous studies demonstrated that zinc finger E-box binding homeobox 2 (ZEB2) may be regulated by miR-30a in clear cell renal cell ca...

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Autores principales: Chen, Xi, Li, Junzheng, Zhang, Shifen, Xu, Weiping, Shi, Dianyu, Zhuo, Mugai, Liang, Shaoqin, Lei, Wenbin, Xie, Chun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6625429/
https://www.ncbi.nlm.nih.gov/pubmed/31257481
http://dx.doi.org/10.3892/mmr.2019.10387
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author Chen, Xi
Li, Junzheng
Zhang, Shifen
Xu, Weiping
Shi, Dianyu
Zhuo, Mugai
Liang, Shaoqin
Lei, Wenbin
Xie, Chun
author_facet Chen, Xi
Li, Junzheng
Zhang, Shifen
Xu, Weiping
Shi, Dianyu
Zhuo, Mugai
Liang, Shaoqin
Lei, Wenbin
Xie, Chun
author_sort Chen, Xi
collection PubMed
description MicroRNA-30a (miR-30a) was previously reported to serve as a tumor suppressor able to inhibit the development and progression of certain types of cancer. A number of previous studies demonstrated that zinc finger E-box binding homeobox 2 (ZEB2) may be regulated by miR-30a in clear cell renal cell carcinoma and breast cancer. However, the function of miR-30a in human nasopharyngeal carcinoma (NPC) remains unclear. The present study aimed to investigate the association between miR-30a and ZEB2 in NPC. Therefore, the expression levels of miR-30a and ZEB2 were measured in human NPC cells and tissues from patients with NPC, and the present results suggested that the expression level of miR-30a was significantly decreased in NPC tissues compared with paracancerous tissues. The direct interaction between miR-30a and the untranslated region of ZEB2 was examined using the dual-luciferase reporter assay, and ZEB2 was identified as a direct target of miR-30a. Additionally, the effects of miR-30a and ZEB2 overexpression on cell proliferation, migration, invasion and apoptosis were additionally investigated. Functional experiments identified that overexpression of miR-30a increased apoptosis and suppressed cell proliferation, cell migration and cell invasion by directly targeting ZEB2. Collectively, the present study suggested that miR-30a may serve an important role in the progression of NPC and may represent a novel target for the treatment of patients with NPC.
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spelling pubmed-66254292019-07-31 MicroRNA-30a regulates cell proliferation, migration, invasion and apoptosis in human nasopharyngeal carcinoma via targeted regulation of ZEB2 Chen, Xi Li, Junzheng Zhang, Shifen Xu, Weiping Shi, Dianyu Zhuo, Mugai Liang, Shaoqin Lei, Wenbin Xie, Chun Mol Med Rep Articles MicroRNA-30a (miR-30a) was previously reported to serve as a tumor suppressor able to inhibit the development and progression of certain types of cancer. A number of previous studies demonstrated that zinc finger E-box binding homeobox 2 (ZEB2) may be regulated by miR-30a in clear cell renal cell carcinoma and breast cancer. However, the function of miR-30a in human nasopharyngeal carcinoma (NPC) remains unclear. The present study aimed to investigate the association between miR-30a and ZEB2 in NPC. Therefore, the expression levels of miR-30a and ZEB2 were measured in human NPC cells and tissues from patients with NPC, and the present results suggested that the expression level of miR-30a was significantly decreased in NPC tissues compared with paracancerous tissues. The direct interaction between miR-30a and the untranslated region of ZEB2 was examined using the dual-luciferase reporter assay, and ZEB2 was identified as a direct target of miR-30a. Additionally, the effects of miR-30a and ZEB2 overexpression on cell proliferation, migration, invasion and apoptosis were additionally investigated. Functional experiments identified that overexpression of miR-30a increased apoptosis and suppressed cell proliferation, cell migration and cell invasion by directly targeting ZEB2. Collectively, the present study suggested that miR-30a may serve an important role in the progression of NPC and may represent a novel target for the treatment of patients with NPC. D.A. Spandidos 2019-08 2019-06-14 /pmc/articles/PMC6625429/ /pubmed/31257481 http://dx.doi.org/10.3892/mmr.2019.10387 Text en Copyright: © Chen et al. 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
Chen, Xi
Li, Junzheng
Zhang, Shifen
Xu, Weiping
Shi, Dianyu
Zhuo, Mugai
Liang, Shaoqin
Lei, Wenbin
Xie, Chun
MicroRNA-30a regulates cell proliferation, migration, invasion and apoptosis in human nasopharyngeal carcinoma via targeted regulation of ZEB2
title MicroRNA-30a regulates cell proliferation, migration, invasion and apoptosis in human nasopharyngeal carcinoma via targeted regulation of ZEB2
title_full MicroRNA-30a regulates cell proliferation, migration, invasion and apoptosis in human nasopharyngeal carcinoma via targeted regulation of ZEB2
title_fullStr MicroRNA-30a regulates cell proliferation, migration, invasion and apoptosis in human nasopharyngeal carcinoma via targeted regulation of ZEB2
title_full_unstemmed MicroRNA-30a regulates cell proliferation, migration, invasion and apoptosis in human nasopharyngeal carcinoma via targeted regulation of ZEB2
title_short MicroRNA-30a regulates cell proliferation, migration, invasion and apoptosis in human nasopharyngeal carcinoma via targeted regulation of ZEB2
title_sort microrna-30a regulates cell proliferation, migration, invasion and apoptosis in human nasopharyngeal carcinoma via targeted regulation of zeb2
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6625429/
https://www.ncbi.nlm.nih.gov/pubmed/31257481
http://dx.doi.org/10.3892/mmr.2019.10387
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