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miR-125a-5p inhibits colorectal cancer cell epithelial–mesenchymal transition, invasion and migration by targeting TAZ

Background: miR-125a-5p regulated biological processes in various types of cancer, including colorectal cancer (CRC). TAZ, a vital transcriptional coactivators of the Hippo pathway, was found to be overexpressed in various cancers. Objectives: This study aims to study the effect of miR-125a-5p on th...

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Autores principales: Tang, Lei, Zhou, Li, Wu, Shengchun, Shi, Xiaoming, Jiang, Guangwei, Niu, Shuai, Ding, Dianzhu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6511622/
https://www.ncbi.nlm.nih.gov/pubmed/31190857
http://dx.doi.org/10.2147/OTT.S191247
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author Tang, Lei
Zhou, Li
Wu, Shengchun
Shi, Xiaoming
Jiang, Guangwei
Niu, Shuai
Ding, Dianzhu
author_facet Tang, Lei
Zhou, Li
Wu, Shengchun
Shi, Xiaoming
Jiang, Guangwei
Niu, Shuai
Ding, Dianzhu
author_sort Tang, Lei
collection PubMed
description Background: miR-125a-5p regulated biological processes in various types of cancer, including colorectal cancer (CRC). TAZ, a vital transcriptional coactivators of the Hippo pathway, was found to be overexpressed in various cancers. Objectives: This study aims to study the effect of miR-125a-5p on the progression of CRC by regulating TAZ expression. Methods: In this study, miR-125a-5p and TAZ expression in CRC tissue and cell lines were detected by real-time polymerase chain reaction (RT-PCR). Luciferase reporter assay was applied to detect whether TAZ was a target of miR-125a-5p. Cell migration and invasion were detected in vitro by wound-healing assay and cell invasion assay. Western blot was used to detect the expression of epithelial-mesenchymal transition (EMT)-related proteins. Findings: The results revealed downregulation of miR-125a-5p, as well as upregulation of TAZ in CRC tissue and cell lines. TAZ was identified as a direct target of miR-125a-5p, and its expression was negatively regulated by miR-125a-5p in CRC cell lines. The functional studies revealed that overexpression of miR-125a-5p inhibited the migration, invasion and EMT of CRC cells, while upregulation of TAZ reversed the inhibitory effect caused by miR-125a-5p. Conclusion: Our data suggest that miR-125a-5p inhibits CRC cell migration, invasion and EMT by targeting TAZ. These results suggest that miR-125a-5p serves as a potential therapeutic biomarker for CRC patients.
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spelling pubmed-65116222019-06-12 miR-125a-5p inhibits colorectal cancer cell epithelial–mesenchymal transition, invasion and migration by targeting TAZ Tang, Lei Zhou, Li Wu, Shengchun Shi, Xiaoming Jiang, Guangwei Niu, Shuai Ding, Dianzhu Onco Targets Ther Original Research Background: miR-125a-5p regulated biological processes in various types of cancer, including colorectal cancer (CRC). TAZ, a vital transcriptional coactivators of the Hippo pathway, was found to be overexpressed in various cancers. Objectives: This study aims to study the effect of miR-125a-5p on the progression of CRC by regulating TAZ expression. Methods: In this study, miR-125a-5p and TAZ expression in CRC tissue and cell lines were detected by real-time polymerase chain reaction (RT-PCR). Luciferase reporter assay was applied to detect whether TAZ was a target of miR-125a-5p. Cell migration and invasion were detected in vitro by wound-healing assay and cell invasion assay. Western blot was used to detect the expression of epithelial-mesenchymal transition (EMT)-related proteins. Findings: The results revealed downregulation of miR-125a-5p, as well as upregulation of TAZ in CRC tissue and cell lines. TAZ was identified as a direct target of miR-125a-5p, and its expression was negatively regulated by miR-125a-5p in CRC cell lines. The functional studies revealed that overexpression of miR-125a-5p inhibited the migration, invasion and EMT of CRC cells, while upregulation of TAZ reversed the inhibitory effect caused by miR-125a-5p. Conclusion: Our data suggest that miR-125a-5p inhibits CRC cell migration, invasion and EMT by targeting TAZ. These results suggest that miR-125a-5p serves as a potential therapeutic biomarker for CRC patients. Dove 2019-05-07 /pmc/articles/PMC6511622/ /pubmed/31190857 http://dx.doi.org/10.2147/OTT.S191247 Text en © 2019 Tang 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
Tang, Lei
Zhou, Li
Wu, Shengchun
Shi, Xiaoming
Jiang, Guangwei
Niu, Shuai
Ding, Dianzhu
miR-125a-5p inhibits colorectal cancer cell epithelial–mesenchymal transition, invasion and migration by targeting TAZ
title miR-125a-5p inhibits colorectal cancer cell epithelial–mesenchymal transition, invasion and migration by targeting TAZ
title_full miR-125a-5p inhibits colorectal cancer cell epithelial–mesenchymal transition, invasion and migration by targeting TAZ
title_fullStr miR-125a-5p inhibits colorectal cancer cell epithelial–mesenchymal transition, invasion and migration by targeting TAZ
title_full_unstemmed miR-125a-5p inhibits colorectal cancer cell epithelial–mesenchymal transition, invasion and migration by targeting TAZ
title_short miR-125a-5p inhibits colorectal cancer cell epithelial–mesenchymal transition, invasion and migration by targeting TAZ
title_sort mir-125a-5p inhibits colorectal cancer cell epithelial–mesenchymal transition, invasion and migration by targeting taz
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6511622/
https://www.ncbi.nlm.nih.gov/pubmed/31190857
http://dx.doi.org/10.2147/OTT.S191247
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