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H19 Knockdown Suppresses Proliferation and Induces Apoptosis by Regulating miR-130a-3p/SATB1 in Breast Cancer Cells

PURPOSE: Breast cancer (BC) is the most common cancer in women. Emerging evidence has demonstrated that lncRNAs play an important role in BC. The objective of this study was to investigate the impact of the long non-coding RNA (lncRNA), H19/miRNA-130a-3P/special AT-rich sequence-binding protein-1 (S...

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Autores principales: Zhong, Guobin, Lin, Yuansheng, Wang, Xu, Wang, Keqiong, Liu, Jianlun, Wei, Wei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7733342/
https://www.ncbi.nlm.nih.gov/pubmed/33324070
http://dx.doi.org/10.2147/OTT.S280142
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author Zhong, Guobin
Lin, Yuansheng
Wang, Xu
Wang, Keqiong
Liu, Jianlun
Wei, Wei
author_facet Zhong, Guobin
Lin, Yuansheng
Wang, Xu
Wang, Keqiong
Liu, Jianlun
Wei, Wei
author_sort Zhong, Guobin
collection PubMed
description PURPOSE: Breast cancer (BC) is the most common cancer in women. Emerging evidence has demonstrated that lncRNAs play an important role in BC. The objective of this study was to investigate the impact of the long non-coding RNA (lncRNA), H19/miRNA-130a-3P/special AT-rich sequence-binding protein-1 (SATB1) axis on BC progression. MATERIALS AND METHODS: Expression of lncRNA and RNA was quantified via RT-qPCR. CCK-8, colony formation, wound healing, transwell, and flow cytometric analyses were used to analyze the proliferation, migration, invasion and apoptosis of cells. A dual-luciferase reporter assay and a RNA immunoprecipitation (RIP) assay were used to assess molecular binding. Protein levels were measured by Western blotting. The function of the lncRNA H19 (hereafter referred to as H19) was examined by xenotransplantation. RESULTS: We demonstrated that H19 expression was higher in cancer tissues and cancer cell lines than in adjacent non-tumor tissues and normal cell lines, respectively. H19 silencing inhibited the proliferation, migration and invasion of BC cells, and induced apoptosis. In addition, H19 directly bound to miR-130a-3p and downregulated its expression. We further demonstrated that H19 sponged miRNA-130a-3p, which resulted in SATB1 upregulation, thus promoting BC progression. Silencing of H19 substantially suppressed BC tumorigenesis in vivo. CONCLUSION: Our data uncovered a novel mechanism of BC progression based on the H19-miR-130a-3p-SATB1 axis.
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spelling pubmed-77333422020-12-14 H19 Knockdown Suppresses Proliferation and Induces Apoptosis by Regulating miR-130a-3p/SATB1 in Breast Cancer Cells Zhong, Guobin Lin, Yuansheng Wang, Xu Wang, Keqiong Liu, Jianlun Wei, Wei Onco Targets Ther Original Research PURPOSE: Breast cancer (BC) is the most common cancer in women. Emerging evidence has demonstrated that lncRNAs play an important role in BC. The objective of this study was to investigate the impact of the long non-coding RNA (lncRNA), H19/miRNA-130a-3P/special AT-rich sequence-binding protein-1 (SATB1) axis on BC progression. MATERIALS AND METHODS: Expression of lncRNA and RNA was quantified via RT-qPCR. CCK-8, colony formation, wound healing, transwell, and flow cytometric analyses were used to analyze the proliferation, migration, invasion and apoptosis of cells. A dual-luciferase reporter assay and a RNA immunoprecipitation (RIP) assay were used to assess molecular binding. Protein levels were measured by Western blotting. The function of the lncRNA H19 (hereafter referred to as H19) was examined by xenotransplantation. RESULTS: We demonstrated that H19 expression was higher in cancer tissues and cancer cell lines than in adjacent non-tumor tissues and normal cell lines, respectively. H19 silencing inhibited the proliferation, migration and invasion of BC cells, and induced apoptosis. In addition, H19 directly bound to miR-130a-3p and downregulated its expression. We further demonstrated that H19 sponged miRNA-130a-3p, which resulted in SATB1 upregulation, thus promoting BC progression. Silencing of H19 substantially suppressed BC tumorigenesis in vivo. CONCLUSION: Our data uncovered a novel mechanism of BC progression based on the H19-miR-130a-3p-SATB1 axis. Dove 2020-12-07 /pmc/articles/PMC7733342/ /pubmed/33324070 http://dx.doi.org/10.2147/OTT.S280142 Text en © 2020 Zhong et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).
spellingShingle Original Research
Zhong, Guobin
Lin, Yuansheng
Wang, Xu
Wang, Keqiong
Liu, Jianlun
Wei, Wei
H19 Knockdown Suppresses Proliferation and Induces Apoptosis by Regulating miR-130a-3p/SATB1 in Breast Cancer Cells
title H19 Knockdown Suppresses Proliferation and Induces Apoptosis by Regulating miR-130a-3p/SATB1 in Breast Cancer Cells
title_full H19 Knockdown Suppresses Proliferation and Induces Apoptosis by Regulating miR-130a-3p/SATB1 in Breast Cancer Cells
title_fullStr H19 Knockdown Suppresses Proliferation and Induces Apoptosis by Regulating miR-130a-3p/SATB1 in Breast Cancer Cells
title_full_unstemmed H19 Knockdown Suppresses Proliferation and Induces Apoptosis by Regulating miR-130a-3p/SATB1 in Breast Cancer Cells
title_short H19 Knockdown Suppresses Proliferation and Induces Apoptosis by Regulating miR-130a-3p/SATB1 in Breast Cancer Cells
title_sort h19 knockdown suppresses proliferation and induces apoptosis by regulating mir-130a-3p/satb1 in breast cancer cells
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7733342/
https://www.ncbi.nlm.nih.gov/pubmed/33324070
http://dx.doi.org/10.2147/OTT.S280142
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