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Lnc‐NA inhibits proliferation and metastasis in endometrioid endometrial carcinoma through regulation of NR4A1
Endometrioid endometrial carcinoma (EEC) is the most common gynaecologic malignancy worldwide. Long non‐coding RNAs have previously been demonstrated to play important roles in regulating human diseases, particularly cancer. However, the biological functions and molecular mechanisms of long non‐codi...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6584524/ https://www.ncbi.nlm.nih.gov/pubmed/31050196 http://dx.doi.org/10.1111/jcmm.14345 |
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author | Sun, Linying Zhou, Rongfang Dong, Jing Liu, Shuang Jiao, Yulian Wang, Laicheng Hu, Shengnan He, Pengjuan Liu, Xiaowen Zhao, Xingbo Jiang, Guosheng Zhao, Yueran |
author_facet | Sun, Linying Zhou, Rongfang Dong, Jing Liu, Shuang Jiao, Yulian Wang, Laicheng Hu, Shengnan He, Pengjuan Liu, Xiaowen Zhao, Xingbo Jiang, Guosheng Zhao, Yueran |
author_sort | Sun, Linying |
collection | PubMed |
description | Endometrioid endometrial carcinoma (EEC) is the most common gynaecologic malignancy worldwide. Long non‐coding RNAs have previously been demonstrated to play important roles in regulating human diseases, particularly cancer. However, the biological functions and molecular mechanisms of long non‐coding RNAs in EEC have not been extensively studied. Here, we describe the discovery of Lnc‐NA from the promoter of the transcription factor nuclear receptor subfamily 4 group A member 1 (NR4A1) gene. The role and function of Lnc‐NA in EEC remain unknown. In this study, we used quantitative real‐time polymerase chain reactions to confirm that Lnc‐NA expression was down‐regulated in 30 EEC cases (90%) and in EEC cell lines compared with that in the paired adjacent tissues and normal endometrial cells. In vitro experiments further demonstrated that overexpressing Lnc‐NA decreased EEC cell proliferation, migration and invasion and promoted apoptosis via inactivation of the apoptosis signalling pathway. Moreover, the results show that Lnc‐NA expression was positively correlated with NR4A1. Furthermore, Lnc‐NA regulated NR4A1 expression and activated the apoptosis signalling pathway to inhibit tumour progression. In summary, our results demonstrate that the Lnc‐NA‐NR4A1 axis could be a useful tumour suppressor and a promising therapeutic target for EEC. |
format | Online Article Text |
id | pubmed-6584524 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-65845242019-07-01 Lnc‐NA inhibits proliferation and metastasis in endometrioid endometrial carcinoma through regulation of NR4A1 Sun, Linying Zhou, Rongfang Dong, Jing Liu, Shuang Jiao, Yulian Wang, Laicheng Hu, Shengnan He, Pengjuan Liu, Xiaowen Zhao, Xingbo Jiang, Guosheng Zhao, Yueran J Cell Mol Med Original Articles Endometrioid endometrial carcinoma (EEC) is the most common gynaecologic malignancy worldwide. Long non‐coding RNAs have previously been demonstrated to play important roles in regulating human diseases, particularly cancer. However, the biological functions and molecular mechanisms of long non‐coding RNAs in EEC have not been extensively studied. Here, we describe the discovery of Lnc‐NA from the promoter of the transcription factor nuclear receptor subfamily 4 group A member 1 (NR4A1) gene. The role and function of Lnc‐NA in EEC remain unknown. In this study, we used quantitative real‐time polymerase chain reactions to confirm that Lnc‐NA expression was down‐regulated in 30 EEC cases (90%) and in EEC cell lines compared with that in the paired adjacent tissues and normal endometrial cells. In vitro experiments further demonstrated that overexpressing Lnc‐NA decreased EEC cell proliferation, migration and invasion and promoted apoptosis via inactivation of the apoptosis signalling pathway. Moreover, the results show that Lnc‐NA expression was positively correlated with NR4A1. Furthermore, Lnc‐NA regulated NR4A1 expression and activated the apoptosis signalling pathway to inhibit tumour progression. In summary, our results demonstrate that the Lnc‐NA‐NR4A1 axis could be a useful tumour suppressor and a promising therapeutic target for EEC. John Wiley and Sons Inc. 2019-05-03 2019-07 /pmc/articles/PMC6584524/ /pubmed/31050196 http://dx.doi.org/10.1111/jcmm.14345 Text en © 2019 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 Sun, Linying Zhou, Rongfang Dong, Jing Liu, Shuang Jiao, Yulian Wang, Laicheng Hu, Shengnan He, Pengjuan Liu, Xiaowen Zhao, Xingbo Jiang, Guosheng Zhao, Yueran Lnc‐NA inhibits proliferation and metastasis in endometrioid endometrial carcinoma through regulation of NR4A1 |
title | Lnc‐NA inhibits proliferation and metastasis in endometrioid endometrial carcinoma through regulation of NR4A1 |
title_full | Lnc‐NA inhibits proliferation and metastasis in endometrioid endometrial carcinoma through regulation of NR4A1 |
title_fullStr | Lnc‐NA inhibits proliferation and metastasis in endometrioid endometrial carcinoma through regulation of NR4A1 |
title_full_unstemmed | Lnc‐NA inhibits proliferation and metastasis in endometrioid endometrial carcinoma through regulation of NR4A1 |
title_short | Lnc‐NA inhibits proliferation and metastasis in endometrioid endometrial carcinoma through regulation of NR4A1 |
title_sort | lnc‐na inhibits proliferation and metastasis in endometrioid endometrial carcinoma through regulation of nr4a1 |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6584524/ https://www.ncbi.nlm.nih.gov/pubmed/31050196 http://dx.doi.org/10.1111/jcmm.14345 |
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