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MiR-369-3p participates in endometrioid adenocarcinoma via the regulation of autophagy

BACKGROUND: The aim of this study is to examine miRNA profiling and miR-369-3p participates in endometrioid adenocarcinoma (EEC) via the regulation of autophagy. METHODS: EEC and its adjacent normal tissues were obtained from 20 clinical patients after surgery. MiRNA profiling was performed using ne...

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Autores principales: Liu, Ping, Ma, Chengbin, Wu, Qiongwei, Zhang, Wenying, Wang, Cao, Yuan, Li, Xi, Xiaowei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6624956/
https://www.ncbi.nlm.nih.gov/pubmed/31337985
http://dx.doi.org/10.1186/s12935-019-0897-8
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author Liu, Ping
Ma, Chengbin
Wu, Qiongwei
Zhang, Wenying
Wang, Cao
Yuan, Li
Xi, Xiaowei
author_facet Liu, Ping
Ma, Chengbin
Wu, Qiongwei
Zhang, Wenying
Wang, Cao
Yuan, Li
Xi, Xiaowei
author_sort Liu, Ping
collection PubMed
description BACKGROUND: The aim of this study is to examine miRNA profiling and miR-369-3p participates in endometrioid adenocarcinoma (EEC) via the regulation of autophagy. METHODS: EEC and its adjacent normal tissues were obtained from 20 clinical patients after surgery. MiRNA profiling was performed using next generation sequencing (NGS) and was validated with quantitative real time PCR (qRT-PCR). qRT-PCR was also employed to measure miR-369-3p and autophagy-related protein 10 (ATG10) expression levels. Western blotting assay was performed to measure the expressions of ATG10 and LC3B. Luciferase reporter assay was conducted to confirm the direct targeting of ATG10 by miR-369-3p. Cell proliferation and migration assays were utilized to analyze the role of miR-369-3p in HEC-1-A cells. RESULTS: We found that miR-369-3p expression levels were down-regulated in EEC compared to the control tissues. The overexpression of miR-369-3p inhibited cell proliferation and migration in EEC; furthermore, ATG10 expression increased in EEC tissues. ATG10 was found to be a potential target of miR-369-3p via a dual-luciferase reporter assay, and ATG10 was shown to be down-regulated by miR-369-3p in protein levels. CONCLUSIONS: This study revealed that miR-369-3p inhibited cell proliferation and migration by targeting ATG10 via autophagy in EEC. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12935-019-0897-8) contains supplementary material, which is available to authorized users.
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spelling pubmed-66249562019-07-23 MiR-369-3p participates in endometrioid adenocarcinoma via the regulation of autophagy Liu, Ping Ma, Chengbin Wu, Qiongwei Zhang, Wenying Wang, Cao Yuan, Li Xi, Xiaowei Cancer Cell Int Primary Research BACKGROUND: The aim of this study is to examine miRNA profiling and miR-369-3p participates in endometrioid adenocarcinoma (EEC) via the regulation of autophagy. METHODS: EEC and its adjacent normal tissues were obtained from 20 clinical patients after surgery. MiRNA profiling was performed using next generation sequencing (NGS) and was validated with quantitative real time PCR (qRT-PCR). qRT-PCR was also employed to measure miR-369-3p and autophagy-related protein 10 (ATG10) expression levels. Western blotting assay was performed to measure the expressions of ATG10 and LC3B. Luciferase reporter assay was conducted to confirm the direct targeting of ATG10 by miR-369-3p. Cell proliferation and migration assays were utilized to analyze the role of miR-369-3p in HEC-1-A cells. RESULTS: We found that miR-369-3p expression levels were down-regulated in EEC compared to the control tissues. The overexpression of miR-369-3p inhibited cell proliferation and migration in EEC; furthermore, ATG10 expression increased in EEC tissues. ATG10 was found to be a potential target of miR-369-3p via a dual-luciferase reporter assay, and ATG10 was shown to be down-regulated by miR-369-3p in protein levels. CONCLUSIONS: This study revealed that miR-369-3p inhibited cell proliferation and migration by targeting ATG10 via autophagy in EEC. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12935-019-0897-8) contains supplementary material, which is available to authorized users. BioMed Central 2019-07-11 /pmc/articles/PMC6624956/ /pubmed/31337985 http://dx.doi.org/10.1186/s12935-019-0897-8 Text en © The Author(s) 2019 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Primary Research
Liu, Ping
Ma, Chengbin
Wu, Qiongwei
Zhang, Wenying
Wang, Cao
Yuan, Li
Xi, Xiaowei
MiR-369-3p participates in endometrioid adenocarcinoma via the regulation of autophagy
title MiR-369-3p participates in endometrioid adenocarcinoma via the regulation of autophagy
title_full MiR-369-3p participates in endometrioid adenocarcinoma via the regulation of autophagy
title_fullStr MiR-369-3p participates in endometrioid adenocarcinoma via the regulation of autophagy
title_full_unstemmed MiR-369-3p participates in endometrioid adenocarcinoma via the regulation of autophagy
title_short MiR-369-3p participates in endometrioid adenocarcinoma via the regulation of autophagy
title_sort mir-369-3p participates in endometrioid adenocarcinoma via the regulation of autophagy
topic Primary Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6624956/
https://www.ncbi.nlm.nih.gov/pubmed/31337985
http://dx.doi.org/10.1186/s12935-019-0897-8
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