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MiR‐30a‐5p inhibits proliferation and metastasis of hydatidiform mole by regulating B3GNT5 through ERK/AKT pathways
Hydatidiform moles are gestational trophoblastic disease. They are abnormal proliferations of trophoblast cells that have the potential to become cancerous. miR‐miR30a‐5p is a tumour suppressor that participates in the development of numerous diseases. However, the role of miR‐30a in hydatidiform mo...
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/PMC7412694/ https://www.ncbi.nlm.nih.gov/pubmed/32575164 http://dx.doi.org/10.1111/jcmm.15247 |
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author | Guo, Zhenzhen Sun, Qiannan Liao, Yangyou Liu, Chao Zhao, Wenjie Li, Xiaoxue Liu, Huan Dong, Ming Shang, Yuhong Sui, Linlin Kong, Ying |
author_facet | Guo, Zhenzhen Sun, Qiannan Liao, Yangyou Liu, Chao Zhao, Wenjie Li, Xiaoxue Liu, Huan Dong, Ming Shang, Yuhong Sui, Linlin Kong, Ying |
author_sort | Guo, Zhenzhen |
collection | PubMed |
description | Hydatidiform moles are gestational trophoblastic disease. They are abnormal proliferations of trophoblast cells that have the potential to become cancerous. miR‐miR30a‐5p is a tumour suppressor that participates in the development of numerous diseases. However, the role of miR‐30a in hydatidiform moles and the mechanisms underlying its effects are presently unclear. This study explored the levels of miR‐30a and B3GNT5 expression in human hydatidiform mole tissue. The results showed that miR‐30a and B3GNT5 were differentially expressed in normal placenta and hydatidiform mole, and miR‐30a decreased cell proliferation, invasion and migration in trophoblast cell lines. Upon further examination, it was confirmed that miR‐30a directly targeted the 3’untranslated region of B3GNT5 using a dual‐luciferase assay. The results of the present study also revealed that miR‐30a reduced the proliferation, invasion and migration ability in JAR and BeWo cells by regulating B3GNT5, which may inactivate the ERK and AKT signalling pathways. This study demonstrated that miR‐30a was a novel target B3GNT5 that serves an important role in the development of hydatidiform moles, suggesting that miR‐30a may serve as a novel potential biomarker or useful diagnostic and therapeutic tool for hydatidiform moles in clinical settings. |
format | Online Article Text |
id | pubmed-7412694 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-74126942020-08-10 MiR‐30a‐5p inhibits proliferation and metastasis of hydatidiform mole by regulating B3GNT5 through ERK/AKT pathways Guo, Zhenzhen Sun, Qiannan Liao, Yangyou Liu, Chao Zhao, Wenjie Li, Xiaoxue Liu, Huan Dong, Ming Shang, Yuhong Sui, Linlin Kong, Ying J Cell Mol Med Original Articles Hydatidiform moles are gestational trophoblastic disease. They are abnormal proliferations of trophoblast cells that have the potential to become cancerous. miR‐miR30a‐5p is a tumour suppressor that participates in the development of numerous diseases. However, the role of miR‐30a in hydatidiform moles and the mechanisms underlying its effects are presently unclear. This study explored the levels of miR‐30a and B3GNT5 expression in human hydatidiform mole tissue. The results showed that miR‐30a and B3GNT5 were differentially expressed in normal placenta and hydatidiform mole, and miR‐30a decreased cell proliferation, invasion and migration in trophoblast cell lines. Upon further examination, it was confirmed that miR‐30a directly targeted the 3’untranslated region of B3GNT5 using a dual‐luciferase assay. The results of the present study also revealed that miR‐30a reduced the proliferation, invasion and migration ability in JAR and BeWo cells by regulating B3GNT5, which may inactivate the ERK and AKT signalling pathways. This study demonstrated that miR‐30a was a novel target B3GNT5 that serves an important role in the development of hydatidiform moles, suggesting that miR‐30a may serve as a novel potential biomarker or useful diagnostic and therapeutic tool for hydatidiform moles in clinical settings. John Wiley and Sons Inc. 2020-06-23 2020-08 /pmc/articles/PMC7412694/ /pubmed/32575164 http://dx.doi.org/10.1111/jcmm.15247 Text en © 2020 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. 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 Guo, Zhenzhen Sun, Qiannan Liao, Yangyou Liu, Chao Zhao, Wenjie Li, Xiaoxue Liu, Huan Dong, Ming Shang, Yuhong Sui, Linlin Kong, Ying MiR‐30a‐5p inhibits proliferation and metastasis of hydatidiform mole by regulating B3GNT5 through ERK/AKT pathways |
title | MiR‐30a‐5p inhibits proliferation and metastasis of hydatidiform mole by regulating B3GNT5 through ERK/AKT pathways |
title_full | MiR‐30a‐5p inhibits proliferation and metastasis of hydatidiform mole by regulating B3GNT5 through ERK/AKT pathways |
title_fullStr | MiR‐30a‐5p inhibits proliferation and metastasis of hydatidiform mole by regulating B3GNT5 through ERK/AKT pathways |
title_full_unstemmed | MiR‐30a‐5p inhibits proliferation and metastasis of hydatidiform mole by regulating B3GNT5 through ERK/AKT pathways |
title_short | MiR‐30a‐5p inhibits proliferation and metastasis of hydatidiform mole by regulating B3GNT5 through ERK/AKT pathways |
title_sort | mir‐30a‐5p inhibits proliferation and metastasis of hydatidiform mole by regulating b3gnt5 through erk/akt pathways |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7412694/ https://www.ncbi.nlm.nih.gov/pubmed/32575164 http://dx.doi.org/10.1111/jcmm.15247 |
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