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miR-185-3p regulates the invasion and metastasis of nasopharyngeal carcinoma by targeting WNT2B in vitro

MicroRNAs (miRs) have been recognised as important regulators of malignant behaviour in different types of human cancer, including nasopharyngeal carcinoma (NPC). A previous study by our group revealed that miR-185-3p regulates the radioresistance of NPC cells. The present study aimed to investigate...

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Autores principales: Liu, Chao, Li, Guo, Ren, Shuling, Su, Zhongwu, Wang, Yunyun, Tian, Yongquan, Liu, Yong, Qiu, Yuanzheng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5403522/
https://www.ncbi.nlm.nih.gov/pubmed/28454443
http://dx.doi.org/10.3892/ol.2017.5778
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author Liu, Chao
Li, Guo
Ren, Shuling
Su, Zhongwu
Wang, Yunyun
Tian, Yongquan
Liu, Yong
Qiu, Yuanzheng
author_facet Liu, Chao
Li, Guo
Ren, Shuling
Su, Zhongwu
Wang, Yunyun
Tian, Yongquan
Liu, Yong
Qiu, Yuanzheng
author_sort Liu, Chao
collection PubMed
description MicroRNAs (miRs) have been recognised as important regulators of malignant behaviour in different types of human cancer, including nasopharyngeal carcinoma (NPC). A previous study by our group revealed that miR-185-3p regulates the radioresistance of NPC cells. The present study aimed to investigate the effect of miR-185-3p on NPC invasion and metastasis. Human NPC CNE-2 and 5-8F cell lines were transfected with a miR-185-3p mimic and miR-185-3p inhibitor, respectively, and their effects on the invasion and metastasis of these cells was assessed using a wound healing assay and Matrigel invasion assay. The target gene of miR-185-3p, Wnt family member 2B (WNT2B) was silenced in 5-8F cells using siRNA in order to investigate its function in NPC. Data from the present study demonstrated that the expression of miR-185-3p was the highest in 5-8F and lowest in CNE-2 cells out of a range of NPC cell lines. Following the transfection of miR-185-3p mimic into CNE-2 cells, the wound healing and Matrigel invasion assays indicated that the migration and invasion ability of CNE-2 cells was significantly reduced compared with the negative control group. In addition, the inhibition of miR-185-3p in 5-8F cells significantly increased the capacity for migration and invasion. Furthermore, silencing WNT2B expression resulted in a significant reduction in the invasion and metastasis in 5-8F cells. The inhibition of miR-185-3p, which promotes invasion and metastasis, could be reversed through the silencing of WNT2B in 5-8F cells. The results of the present study indicate that miR-185-3p mediates the invasion and metastasis of NPC by targeting WNT2B in vitro.
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spelling pubmed-54035222017-04-27 miR-185-3p regulates the invasion and metastasis of nasopharyngeal carcinoma by targeting WNT2B in vitro Liu, Chao Li, Guo Ren, Shuling Su, Zhongwu Wang, Yunyun Tian, Yongquan Liu, Yong Qiu, Yuanzheng Oncol Lett Articles MicroRNAs (miRs) have been recognised as important regulators of malignant behaviour in different types of human cancer, including nasopharyngeal carcinoma (NPC). A previous study by our group revealed that miR-185-3p regulates the radioresistance of NPC cells. The present study aimed to investigate the effect of miR-185-3p on NPC invasion and metastasis. Human NPC CNE-2 and 5-8F cell lines were transfected with a miR-185-3p mimic and miR-185-3p inhibitor, respectively, and their effects on the invasion and metastasis of these cells was assessed using a wound healing assay and Matrigel invasion assay. The target gene of miR-185-3p, Wnt family member 2B (WNT2B) was silenced in 5-8F cells using siRNA in order to investigate its function in NPC. Data from the present study demonstrated that the expression of miR-185-3p was the highest in 5-8F and lowest in CNE-2 cells out of a range of NPC cell lines. Following the transfection of miR-185-3p mimic into CNE-2 cells, the wound healing and Matrigel invasion assays indicated that the migration and invasion ability of CNE-2 cells was significantly reduced compared with the negative control group. In addition, the inhibition of miR-185-3p in 5-8F cells significantly increased the capacity for migration and invasion. Furthermore, silencing WNT2B expression resulted in a significant reduction in the invasion and metastasis in 5-8F cells. The inhibition of miR-185-3p, which promotes invasion and metastasis, could be reversed through the silencing of WNT2B in 5-8F cells. The results of the present study indicate that miR-185-3p mediates the invasion and metastasis of NPC by targeting WNT2B in vitro. D.A. Spandidos 2017-04 2017-02-24 /pmc/articles/PMC5403522/ /pubmed/28454443 http://dx.doi.org/10.3892/ol.2017.5778 Text en Copyright: © Liu 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
Liu, Chao
Li, Guo
Ren, Shuling
Su, Zhongwu
Wang, Yunyun
Tian, Yongquan
Liu, Yong
Qiu, Yuanzheng
miR-185-3p regulates the invasion and metastasis of nasopharyngeal carcinoma by targeting WNT2B in vitro
title miR-185-3p regulates the invasion and metastasis of nasopharyngeal carcinoma by targeting WNT2B in vitro
title_full miR-185-3p regulates the invasion and metastasis of nasopharyngeal carcinoma by targeting WNT2B in vitro
title_fullStr miR-185-3p regulates the invasion and metastasis of nasopharyngeal carcinoma by targeting WNT2B in vitro
title_full_unstemmed miR-185-3p regulates the invasion and metastasis of nasopharyngeal carcinoma by targeting WNT2B in vitro
title_short miR-185-3p regulates the invasion and metastasis of nasopharyngeal carcinoma by targeting WNT2B in vitro
title_sort mir-185-3p regulates the invasion and metastasis of nasopharyngeal carcinoma by targeting wnt2b in vitro
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5403522/
https://www.ncbi.nlm.nih.gov/pubmed/28454443
http://dx.doi.org/10.3892/ol.2017.5778
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