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MiR-200c promotes bladder cancer cell migration and invasion by directly targeting RECK
BACKGROUND: Increasing evidence suggests that the dysregulation of certain microRNAs plays an important role in tumorigenesis and metastasis. MiR-200c exhibits a disordered expression in many tumors and presents dual roles in bladder cancer (BC). Therefore, the definite role of miR-200c in BC needs...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove Medical Press
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4993393/ https://www.ncbi.nlm.nih.gov/pubmed/27574450 http://dx.doi.org/10.2147/OTT.S101067 |
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author | Cheng, Yidong Zhang, Xiaolei Li, Peng Yang, Chengdi Tang, Jinyuan Deng, Xiaheng Yang, Xiao Tao, Jun Lu, Qiang Li, Pengchao |
author_facet | Cheng, Yidong Zhang, Xiaolei Li, Peng Yang, Chengdi Tang, Jinyuan Deng, Xiaheng Yang, Xiao Tao, Jun Lu, Qiang Li, Pengchao |
author_sort | Cheng, Yidong |
collection | PubMed |
description | BACKGROUND: Increasing evidence suggests that the dysregulation of certain microRNAs plays an important role in tumorigenesis and metastasis. MiR-200c exhibits a disordered expression in many tumors and presents dual roles in bladder cancer (BC). Therefore, the definite role of miR-200c in BC needs to be investigated further. MATERIALS AND METHODS: Quantitative reverse transcription polymerase chain reaction was used to assess miR-200c expression. Cell invasion and migration were evaluated using wound healing and transwell assays. The luciferase reporter assay was used to identify the direct target of miR-200c. The expression of reversion-inducing cysteine-rich protein with kazal motifs (RECK) in BC tissues and adjacent nontumor tissues, as well as in BC cell lines, was detected through quantitative reverse transcription polymerase chain reaction, Western blot assay, and immunohistochemistry. RESULTS: The miR-200c expression was significantly upregulated in the BC tissues compared with the adjacent nontumor tissues. The downregulation of miR-200c significantly inhibited cell migration and invasion in the BC cell lines. The luciferase reporter assay showed that RECK was a direct target of miR-200c. The knockdown of RECK in the BC cell lines treated with anti-miR-200c elevated the previously attenuated cell migration and invasion. CONCLUSION: Our findings indicated that miR-200c functions as oncogenes in BC and may provide a novel therapeutic strategy for the treatment of BC. |
format | Online Article Text |
id | pubmed-4993393 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Dove Medical Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-49933932016-08-29 MiR-200c promotes bladder cancer cell migration and invasion by directly targeting RECK Cheng, Yidong Zhang, Xiaolei Li, Peng Yang, Chengdi Tang, Jinyuan Deng, Xiaheng Yang, Xiao Tao, Jun Lu, Qiang Li, Pengchao Onco Targets Ther Original Research BACKGROUND: Increasing evidence suggests that the dysregulation of certain microRNAs plays an important role in tumorigenesis and metastasis. MiR-200c exhibits a disordered expression in many tumors and presents dual roles in bladder cancer (BC). Therefore, the definite role of miR-200c in BC needs to be investigated further. MATERIALS AND METHODS: Quantitative reverse transcription polymerase chain reaction was used to assess miR-200c expression. Cell invasion and migration were evaluated using wound healing and transwell assays. The luciferase reporter assay was used to identify the direct target of miR-200c. The expression of reversion-inducing cysteine-rich protein with kazal motifs (RECK) in BC tissues and adjacent nontumor tissues, as well as in BC cell lines, was detected through quantitative reverse transcription polymerase chain reaction, Western blot assay, and immunohistochemistry. RESULTS: The miR-200c expression was significantly upregulated in the BC tissues compared with the adjacent nontumor tissues. The downregulation of miR-200c significantly inhibited cell migration and invasion in the BC cell lines. The luciferase reporter assay showed that RECK was a direct target of miR-200c. The knockdown of RECK in the BC cell lines treated with anti-miR-200c elevated the previously attenuated cell migration and invasion. CONCLUSION: Our findings indicated that miR-200c functions as oncogenes in BC and may provide a novel therapeutic strategy for the treatment of BC. Dove Medical Press 2016-08-16 /pmc/articles/PMC4993393/ /pubmed/27574450 http://dx.doi.org/10.2147/OTT.S101067 Text en © 2016 Cheng et al. 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. |
spellingShingle | Original Research Cheng, Yidong Zhang, Xiaolei Li, Peng Yang, Chengdi Tang, Jinyuan Deng, Xiaheng Yang, Xiao Tao, Jun Lu, Qiang Li, Pengchao MiR-200c promotes bladder cancer cell migration and invasion by directly targeting RECK |
title | MiR-200c promotes bladder cancer cell migration and invasion by directly targeting RECK |
title_full | MiR-200c promotes bladder cancer cell migration and invasion by directly targeting RECK |
title_fullStr | MiR-200c promotes bladder cancer cell migration and invasion by directly targeting RECK |
title_full_unstemmed | MiR-200c promotes bladder cancer cell migration and invasion by directly targeting RECK |
title_short | MiR-200c promotes bladder cancer cell migration and invasion by directly targeting RECK |
title_sort | mir-200c promotes bladder cancer cell migration and invasion by directly targeting reck |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4993393/ https://www.ncbi.nlm.nih.gov/pubmed/27574450 http://dx.doi.org/10.2147/OTT.S101067 |
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