MicroRNA-206 suppresses growth and metastasis of breast cancer stem cells via blocking EVI-1-mediated CALR expression

Aim to investigate the effect of miR-206 on the growth and metastasis of breast cancer stem cells and clarify the precise mechanism of miR-206 on EVI-1-mediated CALR expression in driving malignant phenotype. Our results showed that miR-206 mimics suppressed CALR expression, inhibited the proliferat...

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Detalles Bibliográficos
Autores principales: Sun, Dapeng, Li, Chenguang, Zhang, Fengxiang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2022
Materias:
Research Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9498949/
https://www.ncbi.nlm.nih.gov/pubmed/36136972
http://dx.doi.org/10.1371/journal.pone.0274919
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author Sun, Dapeng
Li, Chenguang
Zhang, Fengxiang
author_facet Sun, Dapeng
Li, Chenguang
Zhang, Fengxiang
author_sort Sun, Dapeng
collection PubMed
description Aim to investigate the effect of miR-206 on the growth and metastasis of breast cancer stem cells and clarify the precise mechanism of miR-206 on EVI-1-mediated CALR expression in driving malignant phenotype. Our results showed that miR-206 mimics suppressed CALR expression, inhibited the proliferation and metastasis ability of breast cancer stem cells and finally induced cellular apoptosis. Over-expression of CALR could effectively attenuate the cytotoxic effect of miR-206. Further studies demonstrated that EVI-1 could be served as a key regulator of miR206-mediated CALR expression. Elevation of EVI-1 can reverse the function of miR-206 on induction of CALR.
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spelling pubmed-94989492022-09-23 MicroRNA-206 suppresses growth and metastasis of breast cancer stem cells via blocking EVI-1-mediated CALR expression Sun, Dapeng Li, Chenguang Zhang, Fengxiang PLoS One Research Article Aim to investigate the effect of miR-206 on the growth and metastasis of breast cancer stem cells and clarify the precise mechanism of miR-206 on EVI-1-mediated CALR expression in driving malignant phenotype. Our results showed that miR-206 mimics suppressed CALR expression, inhibited the proliferation and metastasis ability of breast cancer stem cells and finally induced cellular apoptosis. Over-expression of CALR could effectively attenuate the cytotoxic effect of miR-206. Further studies demonstrated that EVI-1 could be served as a key regulator of miR206-mediated CALR expression. Elevation of EVI-1 can reverse the function of miR-206 on induction of CALR. Public Library of Science 2022-09-22 /pmc/articles/PMC9498949/ /pubmed/36136972 http://dx.doi.org/10.1371/journal.pone.0274919 Text en © 2022 Sun et al https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Sun, Dapeng
Li, Chenguang
Zhang, Fengxiang
MicroRNA-206 suppresses growth and metastasis of breast cancer stem cells via blocking EVI-1-mediated CALR expression
title MicroRNA-206 suppresses growth and metastasis of breast cancer stem cells via blocking EVI-1-mediated CALR expression
title_full MicroRNA-206 suppresses growth and metastasis of breast cancer stem cells via blocking EVI-1-mediated CALR expression
title_fullStr MicroRNA-206 suppresses growth and metastasis of breast cancer stem cells via blocking EVI-1-mediated CALR expression
title_full_unstemmed MicroRNA-206 suppresses growth and metastasis of breast cancer stem cells via blocking EVI-1-mediated CALR expression
title_short MicroRNA-206 suppresses growth and metastasis of breast cancer stem cells via blocking EVI-1-mediated CALR expression
title_sort microrna-206 suppresses growth and metastasis of breast cancer stem cells via blocking evi-1-mediated calr expression
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9498949/
https://www.ncbi.nlm.nih.gov/pubmed/36136972
http://dx.doi.org/10.1371/journal.pone.0274919
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