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microRNA-27b inhibits cell proliferation and invasion in bladder cancer by targeting engrailed-2

Background: Bladder cancer is considered a malignant tumour characterised by great heterogeneity. Engrailed-2 may be a gene implicated in bladder cancer. Bioinformatics analysis found base pair complementation between microRNA-27b and engrailed-2. The present study aimed to investigate the reciproca...

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Autores principales: Li, Yunfei, Duan, Qilin, Gan, Lu, Li, Wei, Yang, Jianggen, Huang, Guixiao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Portland Press Ltd. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7791549/
https://www.ncbi.nlm.nih.gov/pubmed/33350453
http://dx.doi.org/10.1042/BSR20201000
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author Li, Yunfei
Duan, Qilin
Gan, Lu
Li, Wei
Yang, Jianggen
Huang, Guixiao
author_facet Li, Yunfei
Duan, Qilin
Gan, Lu
Li, Wei
Yang, Jianggen
Huang, Guixiao
author_sort Li, Yunfei
collection PubMed
description Background: Bladder cancer is considered a malignant tumour characterised by great heterogeneity. Engrailed-2 may be a gene implicated in bladder cancer. Bioinformatics analysis found base pair complementation between microRNA-27b and engrailed-2. The present study aimed to investigate the reciprocal association between microRNA-27b and engrailed-2 in bladder cancer. Methods: The microRNA-27b and the protein of engrailed-2 in the tissues and cells of the bladder were detected. The processes of apoptosis, proliferation, invasion, and migration of tumour cells were evaluated. The co-action between microRNA-27b and engrailed-2 was detected by a luciferase reporter system. Finally, the interaction between microRNA-27b and engrailed-2 was further verified in vivo. Results: The study found that the expression level of microRNA-27b is lower in bladder cancer tissues and cells than that in neighbouring ordinary tissues, whereas the opposite outcome was observed regarding the expression level of engrailed-2. Furthermore, microRNA-27b expression level is not significantly linked to the age of patients with bladder cancer; however, it is significantly associated with the clinicopathological grade of bladder cancer. Notably, engrailed-2 is negatively regulated by microRNA-27b. Transfection with microRNA-27b was associated with a significant reduction in the activity of bladder cancer cells and promoted apoptosis, while engrailed-2 restoration effectively reversed the above effects of microRNA-27b on bladder cancer in vitro and in vivo. Conclusions: In conclusion, engrailed-2 is engaged in the development and process of bladder cancer through the negative mediation of microRNA-27b; additionally, microRNA-27b/engrailed-2 could form a signalling pathway with a significant effect on the process of bladder cancer.
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spelling pubmed-77915492021-02-04 microRNA-27b inhibits cell proliferation and invasion in bladder cancer by targeting engrailed-2 Li, Yunfei Duan, Qilin Gan, Lu Li, Wei Yang, Jianggen Huang, Guixiao Biosci Rep Gene Expression & Regulation Background: Bladder cancer is considered a malignant tumour characterised by great heterogeneity. Engrailed-2 may be a gene implicated in bladder cancer. Bioinformatics analysis found base pair complementation between microRNA-27b and engrailed-2. The present study aimed to investigate the reciprocal association between microRNA-27b and engrailed-2 in bladder cancer. Methods: The microRNA-27b and the protein of engrailed-2 in the tissues and cells of the bladder were detected. The processes of apoptosis, proliferation, invasion, and migration of tumour cells were evaluated. The co-action between microRNA-27b and engrailed-2 was detected by a luciferase reporter system. Finally, the interaction between microRNA-27b and engrailed-2 was further verified in vivo. Results: The study found that the expression level of microRNA-27b is lower in bladder cancer tissues and cells than that in neighbouring ordinary tissues, whereas the opposite outcome was observed regarding the expression level of engrailed-2. Furthermore, microRNA-27b expression level is not significantly linked to the age of patients with bladder cancer; however, it is significantly associated with the clinicopathological grade of bladder cancer. Notably, engrailed-2 is negatively regulated by microRNA-27b. Transfection with microRNA-27b was associated with a significant reduction in the activity of bladder cancer cells and promoted apoptosis, while engrailed-2 restoration effectively reversed the above effects of microRNA-27b on bladder cancer in vitro and in vivo. Conclusions: In conclusion, engrailed-2 is engaged in the development and process of bladder cancer through the negative mediation of microRNA-27b; additionally, microRNA-27b/engrailed-2 could form a signalling pathway with a significant effect on the process of bladder cancer. Portland Press Ltd. 2021-01-07 /pmc/articles/PMC7791549/ /pubmed/33350453 http://dx.doi.org/10.1042/BSR20201000 Text en © 2021 The Author(s). https://creativecommons.org/licenses/by/4.0/ This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY) (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Gene Expression & Regulation
Li, Yunfei
Duan, Qilin
Gan, Lu
Li, Wei
Yang, Jianggen
Huang, Guixiao
microRNA-27b inhibits cell proliferation and invasion in bladder cancer by targeting engrailed-2
title microRNA-27b inhibits cell proliferation and invasion in bladder cancer by targeting engrailed-2
title_full microRNA-27b inhibits cell proliferation and invasion in bladder cancer by targeting engrailed-2
title_fullStr microRNA-27b inhibits cell proliferation and invasion in bladder cancer by targeting engrailed-2
title_full_unstemmed microRNA-27b inhibits cell proliferation and invasion in bladder cancer by targeting engrailed-2
title_short microRNA-27b inhibits cell proliferation and invasion in bladder cancer by targeting engrailed-2
title_sort microrna-27b inhibits cell proliferation and invasion in bladder cancer by targeting engrailed-2
topic Gene Expression & Regulation
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7791549/
https://www.ncbi.nlm.nih.gov/pubmed/33350453
http://dx.doi.org/10.1042/BSR20201000
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