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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...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2018
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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. |
format | Online Article Text |
id | pubmed-5832968 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
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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