miR-129-3p controls centrosome number in metastatic prostate cancer cells by repressing CP110

The centrosome plays a key role in cancer invasion and metastasis. However, it is unclear how abnormal centrosome numbers are regulated when prostate cancer (PCa) cells become metastatic. CP110 was previously described for its contribution of centrosome amplification (CA) and early development of ag...

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Main Authors: Bijnsdorp, Irene V., Hodzic, Jasmina, Lagerweij, Tonny, Westerman, Bart, Krijgsman, Oscar, Broeke, Jurjen, Verweij, Frederik, Nilsson, R. Jonas A., Rozendaal, Lawrence, van Beusechem, Victor W., van Moorselaar, Jeroen A., Wurdinger, Thomas, Geldof, Albert A.
Format: Online
Language:English
Published: Impact Journals LLC 2016
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4941343/
id pubmed-4941343
recordtype oai_dc
spelling pubmed-49413432016-07-19 miR-129-3p controls centrosome number in metastatic prostate cancer cells by repressing CP110 Bijnsdorp, Irene V. Hodzic, Jasmina Lagerweij, Tonny Westerman, Bart Krijgsman, Oscar Broeke, Jurjen Verweij, Frederik Nilsson, R. Jonas A. Rozendaal, Lawrence van Beusechem, Victor W. van Moorselaar, Jeroen A. Wurdinger, Thomas Geldof, Albert A. Research Paper The centrosome plays a key role in cancer invasion and metastasis. However, it is unclear how abnormal centrosome numbers are regulated when prostate cancer (PCa) cells become metastatic. CP110 was previously described for its contribution of centrosome amplification (CA) and early development of aggressive cell behaviour. However its regulation in metastatic cells remains unclear. Here we identified miR-129-3p as a novel metastatic microRNA. CP110 was identified as its target protein. In PCa cells that have metastatic capacity, CP110 expression was repressed by miR-129-3p. High miR-129-3p expression levels increased cell invasion, while increasing CP110 levels decreased cell invasion. Overexpression of CP110 in metastatic PCa cells resulted in a decrease in the number of metastasis. In tissues of PCa patients, low CP110 and high miR-129-3p expression levels correlated with metastasis, but not with the expression of genes related to EMT. Furthermore, overexpression of CP110 in metastatic PCa cells resulted in excessive-CA (E-CA), and a change in F-actin distribution which is in agreement with their reduced metastatic capacity. Our data demonstrate that miR-129-3p functions as a CA gatekeeper in metastatic PCa cells by maintaining pro-metastatic centrosome amplification (CA) and preventing anti-metastatic E-CA. Impact Journals LLC 2016-02-23 /pmc/articles/PMC4941343/ /pubmed/26918338 http://dx.doi.org/10.18632/oncotarget.7572 Text en Copyright: © 2016 Bijnsdorp et al. http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Bijnsdorp, Irene V.
Hodzic, Jasmina
Lagerweij, Tonny
Westerman, Bart
Krijgsman, Oscar
Broeke, Jurjen
Verweij, Frederik
Nilsson, R. Jonas A.
Rozendaal, Lawrence
van Beusechem, Victor W.
van Moorselaar, Jeroen A.
Wurdinger, Thomas
Geldof, Albert A.
spellingShingle Bijnsdorp, Irene V.
Hodzic, Jasmina
Lagerweij, Tonny
Westerman, Bart
Krijgsman, Oscar
Broeke, Jurjen
Verweij, Frederik
Nilsson, R. Jonas A.
Rozendaal, Lawrence
van Beusechem, Victor W.
van Moorselaar, Jeroen A.
Wurdinger, Thomas
Geldof, Albert A.
miR-129-3p controls centrosome number in metastatic prostate cancer cells by repressing CP110
author_facet Bijnsdorp, Irene V.
Hodzic, Jasmina
Lagerweij, Tonny
Westerman, Bart
Krijgsman, Oscar
Broeke, Jurjen
Verweij, Frederik
Nilsson, R. Jonas A.
Rozendaal, Lawrence
van Beusechem, Victor W.
van Moorselaar, Jeroen A.
Wurdinger, Thomas
Geldof, Albert A.
author_sort Bijnsdorp, Irene V.
title miR-129-3p controls centrosome number in metastatic prostate cancer cells by repressing CP110
title_short miR-129-3p controls centrosome number in metastatic prostate cancer cells by repressing CP110
title_full miR-129-3p controls centrosome number in metastatic prostate cancer cells by repressing CP110
title_fullStr miR-129-3p controls centrosome number in metastatic prostate cancer cells by repressing CP110
title_full_unstemmed miR-129-3p controls centrosome number in metastatic prostate cancer cells by repressing CP110
title_sort mir-129-3p controls centrosome number in metastatic prostate cancer cells by repressing cp110
description The centrosome plays a key role in cancer invasion and metastasis. However, it is unclear how abnormal centrosome numbers are regulated when prostate cancer (PCa) cells become metastatic. CP110 was previously described for its contribution of centrosome amplification (CA) and early development of aggressive cell behaviour. However its regulation in metastatic cells remains unclear. Here we identified miR-129-3p as a novel metastatic microRNA. CP110 was identified as its target protein. In PCa cells that have metastatic capacity, CP110 expression was repressed by miR-129-3p. High miR-129-3p expression levels increased cell invasion, while increasing CP110 levels decreased cell invasion. Overexpression of CP110 in metastatic PCa cells resulted in a decrease in the number of metastasis. In tissues of PCa patients, low CP110 and high miR-129-3p expression levels correlated with metastasis, but not with the expression of genes related to EMT. Furthermore, overexpression of CP110 in metastatic PCa cells resulted in excessive-CA (E-CA), and a change in F-actin distribution which is in agreement with their reduced metastatic capacity. Our data demonstrate that miR-129-3p functions as a CA gatekeeper in metastatic PCa cells by maintaining pro-metastatic centrosome amplification (CA) and preventing anti-metastatic E-CA.
publisher Impact Journals LLC
publishDate 2016
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4941343/
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