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MicroRNA 543 suppresses breast cancer cell proliferation, blocks cell cycle and induces cell apoptosis via direct targeting of ERK/MAPK

BACKGROUND: Breast cancer affects millions of people with a high mortality rate throughout the world; microRNA 543 (miR-543) has been reported to suppress progression in some kinds of cancers, but has not been reported in breast cancer. Thus, the purpose of this study is to investigate the function...

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Autores principales: Chen, Po, Xu, Wentao, Luo, Yi, Zhang, Yi, He, Yi, Yang, Shuo, Yuan, Zhijun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5348068/
https://www.ncbi.nlm.nih.gov/pubmed/28331335
http://dx.doi.org/10.2147/OTT.S118366
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author Chen, Po
Xu, Wentao
Luo, Yi
Zhang, Yi
He, Yi
Yang, Shuo
Yuan, Zhijun
author_facet Chen, Po
Xu, Wentao
Luo, Yi
Zhang, Yi
He, Yi
Yang, Shuo
Yuan, Zhijun
author_sort Chen, Po
collection PubMed
description BACKGROUND: Breast cancer affects millions of people with a high mortality rate throughout the world; microRNA 543 (miR-543) has been reported to suppress progression in some kinds of cancers, but has not been reported in breast cancer. Thus, the purpose of this study is to investigate the function of miR-543 in breast cancer cells. METHODS: Two cell lines, MCF-7 and MDA-MB-231, were selected to be the research objects; the miR-543 overexpression and knockdown models were established in the study by transforming miR-543 mimics and miR-543 inhibitor. Real-time polymerase chain reaction, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, Western blot, clone formation and cell flow cytometer assay were used to test the miR-543’s function. Dual-luciferase assay was used for the detection of miR-543 and ERK2 targeting relationship. RESULTS: The results showed that the cell proliferation and cell cycle were inhibited, and the capability of cell apoptosis was upregulated when miR-543 was overexpressed; we found that there was a target relationship between ERK2 and miR-543. Furthermore, downstream factors of mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase-2 (ERK2) pathway, including RSK2 and MSK1, were decreased in miR-543 overexpression model. CONCLUSION: This study provides series evidences to support that breast cancer progression was inhibited by miR-543 via direct targeting of ERK2 in MAPK/ERK signal pathway, which may provide a molecular basis for better treatment for patients.
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spelling pubmed-53480682017-03-22 MicroRNA 543 suppresses breast cancer cell proliferation, blocks cell cycle and induces cell apoptosis via direct targeting of ERK/MAPK Chen, Po Xu, Wentao Luo, Yi Zhang, Yi He, Yi Yang, Shuo Yuan, Zhijun Onco Targets Ther Original Research BACKGROUND: Breast cancer affects millions of people with a high mortality rate throughout the world; microRNA 543 (miR-543) has been reported to suppress progression in some kinds of cancers, but has not been reported in breast cancer. Thus, the purpose of this study is to investigate the function of miR-543 in breast cancer cells. METHODS: Two cell lines, MCF-7 and MDA-MB-231, were selected to be the research objects; the miR-543 overexpression and knockdown models were established in the study by transforming miR-543 mimics and miR-543 inhibitor. Real-time polymerase chain reaction, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, Western blot, clone formation and cell flow cytometer assay were used to test the miR-543’s function. Dual-luciferase assay was used for the detection of miR-543 and ERK2 targeting relationship. RESULTS: The results showed that the cell proliferation and cell cycle were inhibited, and the capability of cell apoptosis was upregulated when miR-543 was overexpressed; we found that there was a target relationship between ERK2 and miR-543. Furthermore, downstream factors of mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase-2 (ERK2) pathway, including RSK2 and MSK1, were decreased in miR-543 overexpression model. CONCLUSION: This study provides series evidences to support that breast cancer progression was inhibited by miR-543 via direct targeting of ERK2 in MAPK/ERK signal pathway, which may provide a molecular basis for better treatment for patients. Dove Medical Press 2017-03-06 /pmc/articles/PMC5348068/ /pubmed/28331335 http://dx.doi.org/10.2147/OTT.S118366 Text en © 2017 Chen et al. 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.
spellingShingle Original Research
Chen, Po
Xu, Wentao
Luo, Yi
Zhang, Yi
He, Yi
Yang, Shuo
Yuan, Zhijun
MicroRNA 543 suppresses breast cancer cell proliferation, blocks cell cycle and induces cell apoptosis via direct targeting of ERK/MAPK
title MicroRNA 543 suppresses breast cancer cell proliferation, blocks cell cycle and induces cell apoptosis via direct targeting of ERK/MAPK
title_full MicroRNA 543 suppresses breast cancer cell proliferation, blocks cell cycle and induces cell apoptosis via direct targeting of ERK/MAPK
title_fullStr MicroRNA 543 suppresses breast cancer cell proliferation, blocks cell cycle and induces cell apoptosis via direct targeting of ERK/MAPK
title_full_unstemmed MicroRNA 543 suppresses breast cancer cell proliferation, blocks cell cycle and induces cell apoptosis via direct targeting of ERK/MAPK
title_short MicroRNA 543 suppresses breast cancer cell proliferation, blocks cell cycle and induces cell apoptosis via direct targeting of ERK/MAPK
title_sort microrna 543 suppresses breast cancer cell proliferation, blocks cell cycle and induces cell apoptosis via direct targeting of erk/mapk
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5348068/
https://www.ncbi.nlm.nih.gov/pubmed/28331335
http://dx.doi.org/10.2147/OTT.S118366
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