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Aberrant Ki‐67 expression through 3′UTR alternative polyadenylation in breast cancers

Ki‐67 (MKI67) is a marker of cellular proliferation of cancer. Here, we show that Ki‐67 is post‐transcriptionally regulated through alternative polyadenylation (APA) and microRNAs in breast cancer. We show that shortening of the Ki‐67 3′UTR results in the loss of the binding sites for the suppressiv...

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Autores principales: Yan, Hong, Tian, Rui, Wang, Wei, Zhang, Min, Wu, Jing, He, Jie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5832968/
https://www.ncbi.nlm.nih.gov/pubmed/29511610
http://dx.doi.org/10.1002/2211-5463.12364
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author Yan, Hong
Tian, Rui
Wang, Wei
Zhang, Min
Wu, Jing
He, Jie
author_facet Yan, Hong
Tian, Rui
Wang, Wei
Zhang, Min
Wu, Jing
He, Jie
author_sort Yan, Hong
collection PubMed
description Ki‐67 (MKI67) is a marker of cellular proliferation of cancer. Here, we show that Ki‐67 is post‐transcriptionally regulated through alternative polyadenylation (APA) and microRNAs in breast cancer. We show that shortening of the Ki‐67 3′UTR results in the loss of the binding sites for the suppressive miRNAs and thus renders the transcript with a shortened 3′UTR insusceptible to miRNA‐mediated suppression. This APA‐mediated shortening of the Ki‐67 3′UTR contributes to increased mRNA stability and enhanced translational efficiency. In summary, our results not only highlight the post‐transcriptional regulation of Ki‐67 involving APA and microRNAs but also suggest that Ki‐67 3′UTR disruption could serve as a molecular marker in breast cancer.
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spelling pubmed-58329682018-03-06 Aberrant Ki‐67 expression through 3′UTR alternative polyadenylation in breast cancers Yan, Hong Tian, Rui Wang, Wei Zhang, Min Wu, Jing He, Jie FEBS Open Bio Research Articles Ki‐67 (MKI67) is a marker of cellular proliferation of cancer. Here, we show that Ki‐67 is post‐transcriptionally regulated through alternative polyadenylation (APA) and microRNAs in breast cancer. We show that shortening of the Ki‐67 3′UTR results in the loss of the binding sites for the suppressive miRNAs and thus renders the transcript with a shortened 3′UTR insusceptible to miRNA‐mediated suppression. This APA‐mediated shortening of the Ki‐67 3′UTR contributes to increased mRNA stability and enhanced translational efficiency. In summary, our results not only highlight the post‐transcriptional regulation of Ki‐67 involving APA and microRNAs but also suggest that Ki‐67 3′UTR disruption could serve as a molecular marker in breast cancer. John Wiley and Sons Inc. 2018-01-26 /pmc/articles/PMC5832968/ /pubmed/29511610 http://dx.doi.org/10.1002/2211-5463.12364 Text en © 2017 The Authors. Published by FEBS Press and John Wiley & Sons Ltd. This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Articles
Yan, Hong
Tian, Rui
Wang, Wei
Zhang, Min
Wu, Jing
He, Jie
Aberrant Ki‐67 expression through 3′UTR alternative polyadenylation in breast cancers
title Aberrant Ki‐67 expression through 3′UTR alternative polyadenylation in breast cancers
title_full Aberrant Ki‐67 expression through 3′UTR alternative polyadenylation in breast cancers
title_fullStr Aberrant Ki‐67 expression through 3′UTR alternative polyadenylation in breast cancers
title_full_unstemmed Aberrant Ki‐67 expression through 3′UTR alternative polyadenylation in breast cancers
title_short Aberrant Ki‐67 expression through 3′UTR alternative polyadenylation in breast cancers
title_sort aberrant ki‐67 expression through 3′utr alternative polyadenylation in breast cancers
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5832968/
https://www.ncbi.nlm.nih.gov/pubmed/29511610
http://dx.doi.org/10.1002/2211-5463.12364
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