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Circ_0007331 knock‐down suppresses the progression of endometriosis via miR‐200c‐3p/HiF‐1α axis
Endometriosis is considered a benign gynaecological disease with cancer‐like characterizations, which has a high incidence among women of reproductive age. However, this disease has so far lacked timely diagnosis and effective treatment owing to its unclear aetiology. In this study, we identified ab...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7686986/ https://www.ncbi.nlm.nih.gov/pubmed/32960511 http://dx.doi.org/10.1111/jcmm.15833 |
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author | Dong, Lan Zhang, Lu Liu, Hua Xie, Meiting Gao, Jing Zhou, Xiaoyan Zhao, Qinghong Zhang, Silin Yang, Jing |
author_facet | Dong, Lan Zhang, Lu Liu, Hua Xie, Meiting Gao, Jing Zhou, Xiaoyan Zhao, Qinghong Zhang, Silin Yang, Jing |
author_sort | Dong, Lan |
collection | PubMed |
description | Endometriosis is considered a benign gynaecological disease with cancer‐like characterizations, which has a high incidence among women of reproductive age. However, this disease has so far lacked timely diagnosis and effective treatment owing to its unclear aetiology. In this study, we identified aberrant high expression of circ_0007331 in ectopic endometrial cells by comparing the endometrial samples from patients with and without endometriosis. Further functional experiments revealed that circ_0007331 knock‐down effectively suppressed the viability, proliferation and invasive capacity of ectopic endometrial cells. Additionally, we attempted to define the molecular mechanism of circ_0007331 in the initiation and progression of endometriosis. Circ_0007331 acted as a miRNA sponge for miR‐200c‐3p to indirectly regulate the function of HIF‐1α, which plays a key role in the local angiogenesis and hypoxic mechanisms of ectopic endometrium. A final in vivo experiment confirmed that circ_0007331 knock‐down could suppress the development of endometriosis through down‐regulating the expression of HIF‐1α. Collectively, we preliminarily characterized the role and possible insights of circ_0007331/miR‐200c‐3p/HIF‐1α axis in the proliferation and invasion of ectopic endometrial cells. We hope that by exploring the potential function and molecular mechanism of circ_0007331, we can increase our biological insight into the pathogenesis of endometriosis, which will bring the new ways for the diagnosis and therapy of this disease. |
format | Online Article Text |
id | pubmed-7686986 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-76869862020-12-03 Circ_0007331 knock‐down suppresses the progression of endometriosis via miR‐200c‐3p/HiF‐1α axis Dong, Lan Zhang, Lu Liu, Hua Xie, Meiting Gao, Jing Zhou, Xiaoyan Zhao, Qinghong Zhang, Silin Yang, Jing J Cell Mol Med Original Articles Endometriosis is considered a benign gynaecological disease with cancer‐like characterizations, which has a high incidence among women of reproductive age. However, this disease has so far lacked timely diagnosis and effective treatment owing to its unclear aetiology. In this study, we identified aberrant high expression of circ_0007331 in ectopic endometrial cells by comparing the endometrial samples from patients with and without endometriosis. Further functional experiments revealed that circ_0007331 knock‐down effectively suppressed the viability, proliferation and invasive capacity of ectopic endometrial cells. Additionally, we attempted to define the molecular mechanism of circ_0007331 in the initiation and progression of endometriosis. Circ_0007331 acted as a miRNA sponge for miR‐200c‐3p to indirectly regulate the function of HIF‐1α, which plays a key role in the local angiogenesis and hypoxic mechanisms of ectopic endometrium. A final in vivo experiment confirmed that circ_0007331 knock‐down could suppress the development of endometriosis through down‐regulating the expression of HIF‐1α. Collectively, we preliminarily characterized the role and possible insights of circ_0007331/miR‐200c‐3p/HIF‐1α axis in the proliferation and invasion of ectopic endometrial cells. We hope that by exploring the potential function and molecular mechanism of circ_0007331, we can increase our biological insight into the pathogenesis of endometriosis, which will bring the new ways for the diagnosis and therapy of this disease. John Wiley and Sons Inc. 2020-09-22 2020-11 /pmc/articles/PMC7686986/ /pubmed/32960511 http://dx.doi.org/10.1111/jcmm.15833 Text en © 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Dong, Lan Zhang, Lu Liu, Hua Xie, Meiting Gao, Jing Zhou, Xiaoyan Zhao, Qinghong Zhang, Silin Yang, Jing Circ_0007331 knock‐down suppresses the progression of endometriosis via miR‐200c‐3p/HiF‐1α axis |
title | Circ_0007331 knock‐down suppresses the progression of endometriosis via miR‐200c‐3p/HiF‐1α axis |
title_full | Circ_0007331 knock‐down suppresses the progression of endometriosis via miR‐200c‐3p/HiF‐1α axis |
title_fullStr | Circ_0007331 knock‐down suppresses the progression of endometriosis via miR‐200c‐3p/HiF‐1α axis |
title_full_unstemmed | Circ_0007331 knock‐down suppresses the progression of endometriosis via miR‐200c‐3p/HiF‐1α axis |
title_short | Circ_0007331 knock‐down suppresses the progression of endometriosis via miR‐200c‐3p/HiF‐1α axis |
title_sort | circ_0007331 knock‐down suppresses the progression of endometriosis via mir‐200c‐3p/hif‐1α axis |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7686986/ https://www.ncbi.nlm.nih.gov/pubmed/32960511 http://dx.doi.org/10.1111/jcmm.15833 |
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