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The long non‐coding RNA PVT1 represses ANGPTL4 transcription through binding with EZH2 in trophoblast cell
Despite progress in diagnostics and treatment for preeclampsia, it remains the foremost cause of maternal and foetal perinatal morbidity and mortality worldwide. Over recent years, various lines of evidence have emphasized long non‐coding RNAs (lncRNAs) which function as an innovative regulator of b...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5783862/ https://www.ncbi.nlm.nih.gov/pubmed/29193797 http://dx.doi.org/10.1111/jcmm.13405 |
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author | Xu, Yetao Lian, Yifan Zhang, Yuanyuan Huang, Shiyun Zuo, Qing Yang, Nana Chen, Yanzi Wu, Dan Sun, Lizhou |
author_facet | Xu, Yetao Lian, Yifan Zhang, Yuanyuan Huang, Shiyun Zuo, Qing Yang, Nana Chen, Yanzi Wu, Dan Sun, Lizhou |
author_sort | Xu, Yetao |
collection | PubMed |
description | Despite progress in diagnostics and treatment for preeclampsia, it remains the foremost cause of maternal and foetal perinatal morbidity and mortality worldwide. Over recent years, various lines of evidence have emphasized long non‐coding RNAs (lncRNAs) which function as an innovative regulator of biological behaviour, as exemplified by proliferation, apoptosis and metastasis. However, the role of lncRNAs has not been well described in preeclampsia. Here, we identified a lncRNA,PVT1, whose expression was down‐regulated in qRT‐PCR analyses in severe preeclampsia. The effects of PVT1 on development were studied after suppression and overexpression of PVT1 in HTR‐8/SVneo and JEG3 cells. PVT1 knockdown notably inhibited cell proliferation and stimulated cell cycle accumulation and apoptosis. Exogenous PVT1 significantly increased cell proliferation. Based on analysis of RNAseq data, we found that PVT1 could affect the expression of numerous genes, and then investigated the function and regulatory mechanism of PVT1 in trophoblast cells. Further mechanistic analyses implied that the action of PVT1 is moderately attributable to its repression of ANGPTL4 via association with the epigenetic repressor Ezh2. Altogether, our study suggests that PVT1 could play an essential role in preeclampsia progression and probably acts as a latent therapeutic marker; thus, it might be a useful prognostic marker when evaluating new therapies for patients with preeclampsia. |
format | Online Article Text |
id | pubmed-5783862 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-57838622018-02-08 The long non‐coding RNA PVT1 represses ANGPTL4 transcription through binding with EZH2 in trophoblast cell Xu, Yetao Lian, Yifan Zhang, Yuanyuan Huang, Shiyun Zuo, Qing Yang, Nana Chen, Yanzi Wu, Dan Sun, Lizhou J Cell Mol Med Original Articles Despite progress in diagnostics and treatment for preeclampsia, it remains the foremost cause of maternal and foetal perinatal morbidity and mortality worldwide. Over recent years, various lines of evidence have emphasized long non‐coding RNAs (lncRNAs) which function as an innovative regulator of biological behaviour, as exemplified by proliferation, apoptosis and metastasis. However, the role of lncRNAs has not been well described in preeclampsia. Here, we identified a lncRNA,PVT1, whose expression was down‐regulated in qRT‐PCR analyses in severe preeclampsia. The effects of PVT1 on development were studied after suppression and overexpression of PVT1 in HTR‐8/SVneo and JEG3 cells. PVT1 knockdown notably inhibited cell proliferation and stimulated cell cycle accumulation and apoptosis. Exogenous PVT1 significantly increased cell proliferation. Based on analysis of RNAseq data, we found that PVT1 could affect the expression of numerous genes, and then investigated the function and regulatory mechanism of PVT1 in trophoblast cells. Further mechanistic analyses implied that the action of PVT1 is moderately attributable to its repression of ANGPTL4 via association with the epigenetic repressor Ezh2. Altogether, our study suggests that PVT1 could play an essential role in preeclampsia progression and probably acts as a latent therapeutic marker; thus, it might be a useful prognostic marker when evaluating new therapies for patients with preeclampsia. John Wiley and Sons Inc. 2017-11-29 2018-02 /pmc/articles/PMC5783862/ /pubmed/29193797 http://dx.doi.org/10.1111/jcmm.13405 Text en © 2017 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 Creative Commons Attribution (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 Xu, Yetao Lian, Yifan Zhang, Yuanyuan Huang, Shiyun Zuo, Qing Yang, Nana Chen, Yanzi Wu, Dan Sun, Lizhou The long non‐coding RNA PVT1 represses ANGPTL4 transcription through binding with EZH2 in trophoblast cell |
title | The long non‐coding RNA
PVT1 represses ANGPTL4 transcription through binding with EZH2 in trophoblast cell |
title_full | The long non‐coding RNA
PVT1 represses ANGPTL4 transcription through binding with EZH2 in trophoblast cell |
title_fullStr | The long non‐coding RNA
PVT1 represses ANGPTL4 transcription through binding with EZH2 in trophoblast cell |
title_full_unstemmed | The long non‐coding RNA
PVT1 represses ANGPTL4 transcription through binding with EZH2 in trophoblast cell |
title_short | The long non‐coding RNA
PVT1 represses ANGPTL4 transcription through binding with EZH2 in trophoblast cell |
title_sort | long non‐coding rna
pvt1 represses angptl4 transcription through binding with ezh2 in trophoblast cell |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5783862/ https://www.ncbi.nlm.nih.gov/pubmed/29193797 http://dx.doi.org/10.1111/jcmm.13405 |
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