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miR‐548ag functions as an oncogene by suppressing MOB1B in the development of obesity‐related endometrial cancer
Obesity is a high‐risk factor in the development of endometrial cancer (EC). Our previous study observed that miR‐548ag was significantly overexpressed in the sera of obese individuals. Here, we report the function of miR‐548ag and its mechanism in promoting the obesity‐related progression of EC. Th...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10067393/ https://www.ncbi.nlm.nih.gov/pubmed/36445107 http://dx.doi.org/10.1111/cas.15679 |
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author | Pang, Huai Wang, Jingzhou Wei, Qianqian Liu, Jie Chu, Xiaolong Yuan, Chenggang Yang, Bingqi Li, Menghuan Ma, Dingling Tang, Yihan Wang, Cuizhe Zhang, Jun |
author_facet | Pang, Huai Wang, Jingzhou Wei, Qianqian Liu, Jie Chu, Xiaolong Yuan, Chenggang Yang, Bingqi Li, Menghuan Ma, Dingling Tang, Yihan Wang, Cuizhe Zhang, Jun |
author_sort | Pang, Huai |
collection | PubMed |
description | Obesity is a high‐risk factor in the development of endometrial cancer (EC). Our previous study observed that miR‐548ag was significantly overexpressed in the sera of obese individuals. Here, we report the function of miR‐548ag and its mechanism in promoting the obesity‐related progression of EC. The content of miR‐548ag was increased in the serum of obese EC individuals. Bioinformatics analysis indicated that the survival rate of EC patients with a higher expression of miR‐548ag was significantly reduced. The Mps One Binder Kinase Activator 1B (MOB1B, the core member of the Hippo signaling pathway) is a direct target gene of miR‐548ag, which is inversely correlated with the expression of miR‐548ag. The overexpression of miR‐548ag enhances the proliferation, invasion, and migration, and inhibits apoptosis by downregulating the expression of MOB1B, leading to the deactivation of the Hippo pathway in EC cell lines and contributing to tumor progression in vivo. Our study has established that miR‐548ag functions as an oncogene by suppressing MOB1B in the development of obesity‐related EC. |
format | Online Article Text |
id | pubmed-10067393 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-100673932023-04-04 miR‐548ag functions as an oncogene by suppressing MOB1B in the development of obesity‐related endometrial cancer Pang, Huai Wang, Jingzhou Wei, Qianqian Liu, Jie Chu, Xiaolong Yuan, Chenggang Yang, Bingqi Li, Menghuan Ma, Dingling Tang, Yihan Wang, Cuizhe Zhang, Jun Cancer Sci ORIGINAL ARTICLES Obesity is a high‐risk factor in the development of endometrial cancer (EC). Our previous study observed that miR‐548ag was significantly overexpressed in the sera of obese individuals. Here, we report the function of miR‐548ag and its mechanism in promoting the obesity‐related progression of EC. The content of miR‐548ag was increased in the serum of obese EC individuals. Bioinformatics analysis indicated that the survival rate of EC patients with a higher expression of miR‐548ag was significantly reduced. The Mps One Binder Kinase Activator 1B (MOB1B, the core member of the Hippo signaling pathway) is a direct target gene of miR‐548ag, which is inversely correlated with the expression of miR‐548ag. The overexpression of miR‐548ag enhances the proliferation, invasion, and migration, and inhibits apoptosis by downregulating the expression of MOB1B, leading to the deactivation of the Hippo pathway in EC cell lines and contributing to tumor progression in vivo. Our study has established that miR‐548ag functions as an oncogene by suppressing MOB1B in the development of obesity‐related EC. John Wiley and Sons Inc. 2022-12-23 /pmc/articles/PMC10067393/ /pubmed/36445107 http://dx.doi.org/10.1111/cas.15679 Text en © 2022 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, 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 | ORIGINAL ARTICLES Pang, Huai Wang, Jingzhou Wei, Qianqian Liu, Jie Chu, Xiaolong Yuan, Chenggang Yang, Bingqi Li, Menghuan Ma, Dingling Tang, Yihan Wang, Cuizhe Zhang, Jun miR‐548ag functions as an oncogene by suppressing MOB1B in the development of obesity‐related endometrial cancer |
title |
miR‐548ag functions as an oncogene by suppressing MOB1B in the development of obesity‐related endometrial cancer |
title_full |
miR‐548ag functions as an oncogene by suppressing MOB1B in the development of obesity‐related endometrial cancer |
title_fullStr |
miR‐548ag functions as an oncogene by suppressing MOB1B in the development of obesity‐related endometrial cancer |
title_full_unstemmed |
miR‐548ag functions as an oncogene by suppressing MOB1B in the development of obesity‐related endometrial cancer |
title_short |
miR‐548ag functions as an oncogene by suppressing MOB1B in the development of obesity‐related endometrial cancer |
title_sort | mir‐548ag functions as an oncogene by suppressing mob1b in the development of obesity‐related endometrial cancer |
topic | ORIGINAL ARTICLES |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10067393/ https://www.ncbi.nlm.nih.gov/pubmed/36445107 http://dx.doi.org/10.1111/cas.15679 |
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