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Long Non-Coding RNA BCAR4 Binds to miR-644a and Targets TLX1 to Promote the Progression of Bladder Cancer
BACKGROUND: Bladder cancer is a serious threat to human health. It is meaningful to study the pathogenesis of bladder cancer. Long non-coding RNAs (lncRNAs) are reported to promote or inhibit bladder cancer development. However, the role of lncRNA BCAR4 in the regulation of bladder cancer remains un...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2020
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7102885/ https://www.ncbi.nlm.nih.gov/pubmed/32273720 http://dx.doi.org/10.2147/OTT.S232965 |
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author | Wang, Xiaojing He, Hongchao Rui, Wenbin Xie, Xin Wang, Dawei Zhu, Yu |
author_facet | Wang, Xiaojing He, Hongchao Rui, Wenbin Xie, Xin Wang, Dawei Zhu, Yu |
author_sort | Wang, Xiaojing |
collection | PubMed |
description | BACKGROUND: Bladder cancer is a serious threat to human health. It is meaningful to study the pathogenesis of bladder cancer. Long non-coding RNAs (lncRNAs) are reported to promote or inhibit bladder cancer development. However, the role of lncRNA BCAR4 in the regulation of bladder cancer remains unclear. PURPOSE: This study was to explore the role of lncRNA BCAR4 in the progression of bladder cancer cell. METHODS: RT-PCR was used to examine the expression of BCAR4 and miR-644a. CCK8 assay, colony formation assay, Transwell assay were used to detect the progression of bladder cancer cells after transfecting of indicated plasmids. RESULTS: The expression of BCAR4 was higher in bladder cancer cell lines than normal urothelial cell line. Moreover, the expression of BCAR4 was associated with the advanced stage and metastasis of bladder cancer. Through knockdown of BCAR4, we discovered that knockdown of BCAR4 significantly decreased the proliferation, migration and invasive abilities of bladder cancer cells. Mechanically, we showed that BCAR4 can bind to miR-644a directly and targets TLX1. Moreover, we also showed that miR-644a was also highly expressed in bladder cancer cells and inhibition of miR-644a or overexpression of TLX1 can increased the migration abilities of bladder cancer caused by knockdown of BCAR4. CONCLUSION: We showed that BCAR4 sponged miR-644a to modulate the expression of TLX1 and promote bladder cancer development. |
format | Online Article Text |
id | pubmed-7102885 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-71028852020-04-09 Long Non-Coding RNA BCAR4 Binds to miR-644a and Targets TLX1 to Promote the Progression of Bladder Cancer Wang, Xiaojing He, Hongchao Rui, Wenbin Xie, Xin Wang, Dawei Zhu, Yu Onco Targets Ther Original Research BACKGROUND: Bladder cancer is a serious threat to human health. It is meaningful to study the pathogenesis of bladder cancer. Long non-coding RNAs (lncRNAs) are reported to promote or inhibit bladder cancer development. However, the role of lncRNA BCAR4 in the regulation of bladder cancer remains unclear. PURPOSE: This study was to explore the role of lncRNA BCAR4 in the progression of bladder cancer cell. METHODS: RT-PCR was used to examine the expression of BCAR4 and miR-644a. CCK8 assay, colony formation assay, Transwell assay were used to detect the progression of bladder cancer cells after transfecting of indicated plasmids. RESULTS: The expression of BCAR4 was higher in bladder cancer cell lines than normal urothelial cell line. Moreover, the expression of BCAR4 was associated with the advanced stage and metastasis of bladder cancer. Through knockdown of BCAR4, we discovered that knockdown of BCAR4 significantly decreased the proliferation, migration and invasive abilities of bladder cancer cells. Mechanically, we showed that BCAR4 can bind to miR-644a directly and targets TLX1. Moreover, we also showed that miR-644a was also highly expressed in bladder cancer cells and inhibition of miR-644a or overexpression of TLX1 can increased the migration abilities of bladder cancer caused by knockdown of BCAR4. CONCLUSION: We showed that BCAR4 sponged miR-644a to modulate the expression of TLX1 and promote bladder cancer development. Dove 2020-03-24 /pmc/articles/PMC7102885/ /pubmed/32273720 http://dx.doi.org/10.2147/OTT.S232965 Text en © 2020 Wang 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 Wang, Xiaojing He, Hongchao Rui, Wenbin Xie, Xin Wang, Dawei Zhu, Yu Long Non-Coding RNA BCAR4 Binds to miR-644a and Targets TLX1 to Promote the Progression of Bladder Cancer |
title | Long Non-Coding RNA BCAR4 Binds to miR-644a and Targets TLX1 to Promote the Progression of Bladder Cancer |
title_full | Long Non-Coding RNA BCAR4 Binds to miR-644a and Targets TLX1 to Promote the Progression of Bladder Cancer |
title_fullStr | Long Non-Coding RNA BCAR4 Binds to miR-644a and Targets TLX1 to Promote the Progression of Bladder Cancer |
title_full_unstemmed | Long Non-Coding RNA BCAR4 Binds to miR-644a and Targets TLX1 to Promote the Progression of Bladder Cancer |
title_short | Long Non-Coding RNA BCAR4 Binds to miR-644a and Targets TLX1 to Promote the Progression of Bladder Cancer |
title_sort | long non-coding rna bcar4 binds to mir-644a and targets tlx1 to promote the progression of bladder cancer |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7102885/ https://www.ncbi.nlm.nih.gov/pubmed/32273720 http://dx.doi.org/10.2147/OTT.S232965 |
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