A role for polyploidy in the tumorigenicity of Pim-1-expressing human prostate and mammary epithelial cells.

<h4>Background</h4>Polyploidy is a prominent feature of many human cancers, and it has long been hypothesized that polyploidy may contribute to tumorigenesis by promoting genomic instability. In this study, we investigated whether polyploidy per se induced by a relevant oncogene can prom...

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Autores principales:	Meejeon Roh, Omar E Franco, Simon W Hayward, Riet van der Meer, Sarki A Abdulkadir
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2008
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/f7c3d302cc6643d9942ab3d9f8a02b8d
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spelling	oai:doaj.org-article:f7c3d302cc6643d9942ab3d9f8a02b8d2021-11-25T06:11:51ZA role for polyploidy in the tumorigenicity of Pim-1-expressing human prostate and mammary epithelial cells.1932-620310.1371/journal.pone.0002572https://doaj.org/article/f7c3d302cc6643d9942ab3d9f8a02b8d2008-07-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/18596907/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>Polyploidy is a prominent feature of many human cancers, and it has long been hypothesized that polyploidy may contribute to tumorigenesis by promoting genomic instability. In this study, we investigated whether polyploidy per se induced by a relevant oncogene can promote genomic instability and tumorigenicity in human epithelial cells.<h4>Principal findings</h4>When the oncogenic serine-threonine kinase Pim-1 is overexpressed in immortalized, non-tumorigenic human prostate and mammary epithelial cells, these cells gradually converted to polyploidy and became tumorigenic. To assess the contribution of polyploidy to tumorigenicity, we obtained sorted, matched populations of diploid and polyploid cells expressing equivalent levels of the Pim-1 protein. Spectral karyotyping revealed evidence of emerging numerical and structural chromosomal abnormalities in polyploid cells, supporting the proposition that polyploidy promotes chromosomal instability. Polyploid cells displayed an intact p53/p21 pathway, indicating that the viability of polyploid cells in this system is not dependent on the inactivation of the p53 signaling pathway. Remarkably, only the sorted polyploid cells were tumorigenic in vitro and in vivo.<h4>Conclusions</h4>Our results support the notion that polyploidy can promote chromosomal instability and the initiation of tumorigenesis in human epithelial cells.Meejeon RohOmar E FrancoSimon W HaywardRiet van der MeerSarki A AbdulkadirPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 3, Iss 7, p e2572 (2008)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Meejeon Roh Omar E Franco Simon W Hayward Riet van der Meer Sarki A Abdulkadir A role for polyploidy in the tumorigenicity of Pim-1-expressing human prostate and mammary epithelial cells.
description	<h4>Background</h4>Polyploidy is a prominent feature of many human cancers, and it has long been hypothesized that polyploidy may contribute to tumorigenesis by promoting genomic instability. In this study, we investigated whether polyploidy per se induced by a relevant oncogene can promote genomic instability and tumorigenicity in human epithelial cells.<h4>Principal findings</h4>When the oncogenic serine-threonine kinase Pim-1 is overexpressed in immortalized, non-tumorigenic human prostate and mammary epithelial cells, these cells gradually converted to polyploidy and became tumorigenic. To assess the contribution of polyploidy to tumorigenicity, we obtained sorted, matched populations of diploid and polyploid cells expressing equivalent levels of the Pim-1 protein. Spectral karyotyping revealed evidence of emerging numerical and structural chromosomal abnormalities in polyploid cells, supporting the proposition that polyploidy promotes chromosomal instability. Polyploid cells displayed an intact p53/p21 pathway, indicating that the viability of polyploid cells in this system is not dependent on the inactivation of the p53 signaling pathway. Remarkably, only the sorted polyploid cells were tumorigenic in vitro and in vivo.<h4>Conclusions</h4>Our results support the notion that polyploidy can promote chromosomal instability and the initiation of tumorigenesis in human epithelial cells.
format	article
author	Meejeon Roh Omar E Franco Simon W Hayward Riet van der Meer Sarki A Abdulkadir
author_facet	Meejeon Roh Omar E Franco Simon W Hayward Riet van der Meer Sarki A Abdulkadir
author_sort	Meejeon Roh
title	A role for polyploidy in the tumorigenicity of Pim-1-expressing human prostate and mammary epithelial cells.
title_short	A role for polyploidy in the tumorigenicity of Pim-1-expressing human prostate and mammary epithelial cells.
title_full	A role for polyploidy in the tumorigenicity of Pim-1-expressing human prostate and mammary epithelial cells.
title_fullStr	A role for polyploidy in the tumorigenicity of Pim-1-expressing human prostate and mammary epithelial cells.
title_full_unstemmed	A role for polyploidy in the tumorigenicity of Pim-1-expressing human prostate and mammary epithelial cells.
title_sort	role for polyploidy in the tumorigenicity of pim-1-expressing human prostate and mammary epithelial cells.
publisher	Public Library of Science (PLoS)
publishDate	2008
url	https://doaj.org/article/f7c3d302cc6643d9942ab3d9f8a02b8d
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A role for polyploidy in the tumorigenicity of Pim-1-expressing human prostate and mammary epithelial cells.

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