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A cyclin D1/microRNA 17/20 regulatory feedback loop in control of breast cancer cell proliferation

Decreased expression of specific microRNAs (miRNAs) occurs in human tumors, which suggests a function for miRNAs in tumor suppression. Herein, levels of the miR-17-5p/miR-20a miRNA cluster were inversely correlated to cyclin D1 abundance in human breast tumors and cell lines. MiR-17/20 suppressed br...

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Autores principales: Yu, Zuoren, Wang, Chenguang, Wang, Min, Li, Zhiping, Casimiro, Mathew C., Liu, Manran, Wu, Kongming, Whittle, James, Ju, Xiaoming, Hyslop, Terry, McCue, Peter, Pestell, Richard G.
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2500136/
https://www.ncbi.nlm.nih.gov/pubmed/18695042
http://dx.doi.org/10.1083/jcb.200801079
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author Yu, Zuoren
Wang, Chenguang
Wang, Min
Li, Zhiping
Casimiro, Mathew C.
Liu, Manran
Wu, Kongming
Whittle, James
Ju, Xiaoming
Hyslop, Terry
McCue, Peter
Pestell, Richard G.
author_facet Yu, Zuoren
Wang, Chenguang
Wang, Min
Li, Zhiping
Casimiro, Mathew C.
Liu, Manran
Wu, Kongming
Whittle, James
Ju, Xiaoming
Hyslop, Terry
McCue, Peter
Pestell, Richard G.
author_sort Yu, Zuoren
collection PubMed
description Decreased expression of specific microRNAs (miRNAs) occurs in human tumors, which suggests a function for miRNAs in tumor suppression. Herein, levels of the miR-17-5p/miR-20a miRNA cluster were inversely correlated to cyclin D1 abundance in human breast tumors and cell lines. MiR-17/20 suppressed breast cancer cell proliferation and tumor colony formation by negatively regulating cyclin D1 translation via a conserved 3′ untranslated region miRNA-binding site, thereby inhibiting serum-induced S phase entry. The cell cycle effect of miR-17/20 was abrogated by cyclin D1 siRNA and in cyclin D1–deficient breast cancer cells. Mammary epithelial cell–targeted cyclin D1 expression induced miR-17-5p and miR-20a expression in vivo, and cyclin D1 bound the miR-17/20 cluster promoter regulatory region. In summary, these studies identify a novel cyclin D1/miR-17/20 regulatory feedback loop through which cyclin D1 induces miR-17-5p/miR-20a. In turn, miR-17/20 limits the proliferative function of cyclin D1, thus linking expression of a specific miRNA cluster to the regulation of oncogenesis.
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spelling pubmed-25001362009-02-11 A cyclin D1/microRNA 17/20 regulatory feedback loop in control of breast cancer cell proliferation Yu, Zuoren Wang, Chenguang Wang, Min Li, Zhiping Casimiro, Mathew C. Liu, Manran Wu, Kongming Whittle, James Ju, Xiaoming Hyslop, Terry McCue, Peter Pestell, Richard G. J Cell Biol Research Articles Decreased expression of specific microRNAs (miRNAs) occurs in human tumors, which suggests a function for miRNAs in tumor suppression. Herein, levels of the miR-17-5p/miR-20a miRNA cluster were inversely correlated to cyclin D1 abundance in human breast tumors and cell lines. MiR-17/20 suppressed breast cancer cell proliferation and tumor colony formation by negatively regulating cyclin D1 translation via a conserved 3′ untranslated region miRNA-binding site, thereby inhibiting serum-induced S phase entry. The cell cycle effect of miR-17/20 was abrogated by cyclin D1 siRNA and in cyclin D1–deficient breast cancer cells. Mammary epithelial cell–targeted cyclin D1 expression induced miR-17-5p and miR-20a expression in vivo, and cyclin D1 bound the miR-17/20 cluster promoter regulatory region. In summary, these studies identify a novel cyclin D1/miR-17/20 regulatory feedback loop through which cyclin D1 induces miR-17-5p/miR-20a. In turn, miR-17/20 limits the proliferative function of cyclin D1, thus linking expression of a specific miRNA cluster to the regulation of oncogenesis. The Rockefeller University Press 2008-08-11 /pmc/articles/PMC2500136/ /pubmed/18695042 http://dx.doi.org/10.1083/jcb.200801079 Text en © 2008 Yu et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jcb.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).
spellingShingle Research Articles
Yu, Zuoren
Wang, Chenguang
Wang, Min
Li, Zhiping
Casimiro, Mathew C.
Liu, Manran
Wu, Kongming
Whittle, James
Ju, Xiaoming
Hyslop, Terry
McCue, Peter
Pestell, Richard G.
A cyclin D1/microRNA 17/20 regulatory feedback loop in control of breast cancer cell proliferation
title A cyclin D1/microRNA 17/20 regulatory feedback loop in control of breast cancer cell proliferation
title_full A cyclin D1/microRNA 17/20 regulatory feedback loop in control of breast cancer cell proliferation
title_fullStr A cyclin D1/microRNA 17/20 regulatory feedback loop in control of breast cancer cell proliferation
title_full_unstemmed A cyclin D1/microRNA 17/20 regulatory feedback loop in control of breast cancer cell proliferation
title_short A cyclin D1/microRNA 17/20 regulatory feedback loop in control of breast cancer cell proliferation
title_sort cyclin d1/microrna 17/20 regulatory feedback loop in control of breast cancer cell proliferation
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2500136/
https://www.ncbi.nlm.nih.gov/pubmed/18695042
http://dx.doi.org/10.1083/jcb.200801079
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