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LncRNA GNAS-AS1 facilitates ER(+) breast cancer cells progression by promoting M2 macrophage polarization via regulating miR-433-3p/GATA3 axis
Objective: ER(+) breast cancer is the most common type of breast cancer, which seriously affects the physical and mental health of women. Recently, lncRNAs mediated tumor-associated macrophages (TAM) were identified to involve in tumorigenesis. Therefore, the present study aimed at demonstrating the...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Portland Press Ltd.
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7327181/ https://www.ncbi.nlm.nih.gov/pubmed/32538432 http://dx.doi.org/10.1042/BSR20200626 |
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author | Liu, Shi-Qin Zhou, Zhi-Yang Dong, Xue Guo, Lei Zhang, Ke-Jing |
author_facet | Liu, Shi-Qin Zhou, Zhi-Yang Dong, Xue Guo, Lei Zhang, Ke-Jing |
author_sort | Liu, Shi-Qin |
collection | PubMed |
description | Objective: ER(+) breast cancer is the most common type of breast cancer, which seriously affects the physical and mental health of women. Recently, lncRNAs mediated tumor-associated macrophages (TAM) were identified to involve in tumorigenesis. Therefore, the present study aimed at demonstrating the regulatory network of GNAS-AS1 in TAM-mediated ER(+) breast cancer progress. Methods: The expression levels of genes were evaluated using qRT-PCR. The proportions of polarized macrophages (M1, M2) were assessed by flow cytometry. Cell proliferation, migration and invasion were evaluated by CCK-8, wound healing and transwell assay, respectively. Double-luciferase reporter system was used to detect the interaction between molecules. Western blot was applied to test protein levels. Results: The expression of GNAS-AS1 was obviously increased in ER(+) breast cancer tissues and cell lines, as well as M2 macrophages. GNAS-AS1 facilitated the capabilities of proliferation, migration and invasion of ER(+) breast cancer cells by accelerating M2 macrophage polarization via directly sponging miR-433-3p. GATA3, as a target of miR-433-3p, could positively regulate by GNAS-AS1. Furthermore, either miR-433-3p overexpression or GATA3 knockdown impaired the effects of GNAS-AS1 on M2 macrophage polarization and ER(+) breast cancer cells progression. Conclusion: GNAS-AS1/miR-433-3p/GATA3 axis promoted proliferation, metastasis of ER(+) breast cancer cells by accelerating M2 macrophage polarization. The mechanism may provide a new strategy and target for ER(+) breast cancer treatment. |
format | Online Article Text |
id | pubmed-7327181 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Portland Press Ltd. |
record_format | MEDLINE/PubMed |
spelling | pubmed-73271812020-07-10 LncRNA GNAS-AS1 facilitates ER(+) breast cancer cells progression by promoting M2 macrophage polarization via regulating miR-433-3p/GATA3 axis Liu, Shi-Qin Zhou, Zhi-Yang Dong, Xue Guo, Lei Zhang, Ke-Jing Biosci Rep Cancer Objective: ER(+) breast cancer is the most common type of breast cancer, which seriously affects the physical and mental health of women. Recently, lncRNAs mediated tumor-associated macrophages (TAM) were identified to involve in tumorigenesis. Therefore, the present study aimed at demonstrating the regulatory network of GNAS-AS1 in TAM-mediated ER(+) breast cancer progress. Methods: The expression levels of genes were evaluated using qRT-PCR. The proportions of polarized macrophages (M1, M2) were assessed by flow cytometry. Cell proliferation, migration and invasion were evaluated by CCK-8, wound healing and transwell assay, respectively. Double-luciferase reporter system was used to detect the interaction between molecules. Western blot was applied to test protein levels. Results: The expression of GNAS-AS1 was obviously increased in ER(+) breast cancer tissues and cell lines, as well as M2 macrophages. GNAS-AS1 facilitated the capabilities of proliferation, migration and invasion of ER(+) breast cancer cells by accelerating M2 macrophage polarization via directly sponging miR-433-3p. GATA3, as a target of miR-433-3p, could positively regulate by GNAS-AS1. Furthermore, either miR-433-3p overexpression or GATA3 knockdown impaired the effects of GNAS-AS1 on M2 macrophage polarization and ER(+) breast cancer cells progression. Conclusion: GNAS-AS1/miR-433-3p/GATA3 axis promoted proliferation, metastasis of ER(+) breast cancer cells by accelerating M2 macrophage polarization. The mechanism may provide a new strategy and target for ER(+) breast cancer treatment. Portland Press Ltd. 2020-06-30 /pmc/articles/PMC7327181/ /pubmed/32538432 http://dx.doi.org/10.1042/BSR20200626 Text en © 2020 The Author(s). https://creativecommons.org/licenses/by/4.0/ This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY). |
spellingShingle | Cancer Liu, Shi-Qin Zhou, Zhi-Yang Dong, Xue Guo, Lei Zhang, Ke-Jing LncRNA GNAS-AS1 facilitates ER(+) breast cancer cells progression by promoting M2 macrophage polarization via regulating miR-433-3p/GATA3 axis |
title | LncRNA GNAS-AS1 facilitates ER(+) breast cancer cells progression by promoting M2 macrophage polarization via regulating miR-433-3p/GATA3 axis |
title_full | LncRNA GNAS-AS1 facilitates ER(+) breast cancer cells progression by promoting M2 macrophage polarization via regulating miR-433-3p/GATA3 axis |
title_fullStr | LncRNA GNAS-AS1 facilitates ER(+) breast cancer cells progression by promoting M2 macrophage polarization via regulating miR-433-3p/GATA3 axis |
title_full_unstemmed | LncRNA GNAS-AS1 facilitates ER(+) breast cancer cells progression by promoting M2 macrophage polarization via regulating miR-433-3p/GATA3 axis |
title_short | LncRNA GNAS-AS1 facilitates ER(+) breast cancer cells progression by promoting M2 macrophage polarization via regulating miR-433-3p/GATA3 axis |
title_sort | lncrna gnas-as1 facilitates er(+) breast cancer cells progression by promoting m2 macrophage polarization via regulating mir-433-3p/gata3 axis |
topic | Cancer |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7327181/ https://www.ncbi.nlm.nih.gov/pubmed/32538432 http://dx.doi.org/10.1042/BSR20200626 |
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