HTLV-1 Tax: centrosome amplification and cancer

During interphase, each cell contains a single centrosome that acts as a microtubule organizing center for cellular functions in interphase and in mitosis. Centrosome amplification during the S phase of the cell cycle is a tightly regulated process to ensure that each daughter cell receives the prop...

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Main Authors:	Pumfery, Anne, de la Fuente, Cynthia, Kashanchi, Fatah
Format:	Online
Language:	English
Published:	BioMed Central 2006
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1555608/

id	pubmed-1555608
recordtype	oai_dc
spelling	pubmed-15556082006-08-26 HTLV-1 Tax: centrosome amplification and cancer Pumfery, Anne de la Fuente, Cynthia Kashanchi, Fatah Commentary During interphase, each cell contains a single centrosome that acts as a microtubule organizing center for cellular functions in interphase and in mitosis. Centrosome amplification during the S phase of the cell cycle is a tightly regulated process to ensure that each daughter cell receives the proper complement of the genome. The controls that ensure that centrosomes are duplicated exactly once in the cell cycle are not well understood. In solid tumors and hematological malignancies, centrosome abnormalities resulting in aneuploidy is observed in the majority of cancers. These phenotypes are also observed in cancers induced by viruses, including adult T cell lymphoma which is caused by the human T cell lymphotrophic virus Type 1 (HTLV-1). Several reports have indicated that the HTLV-1 transactivator, Tax, is directly responsible for the centrosomal abnormalities observed in ATL cells. A recent paper in Nature Cell Biology by Ching et al. has shed some new light into how Tax may be inducing centrosome abnormalities. The authors demonstrated that 30% of ATL cells contained more than two centrosomes and expression of Tax alone induced supernumerary centrosomes. A cellular coiled-coil protein, Tax1BP2, was shown to interact with Tax and disruption of this interaction led to failure of Tax to induce centrosome amplification. Additionally, down-regulation of Tax1BP2 led to centrosome amplification. These results suggest that Tax1BP2 may be an important block to centrosome re-duplication that is observed in normal cells. Presently, a specific cellular protein that prevents centrosome re-duplication has not been identified. This paper has provided further insight into how Tax induces centrosome abnormalities that lead to ATL. Lastly, additional work on Tax1BP2 will also provide insight into how the cell suppresses centrosome re-duplication during the cell cycle and the role that Tax1BP2 plays in this important cellular pathway. BioMed Central 2006-08-09 /pmc/articles/PMC1555608/ /pubmed/16899128 http://dx.doi.org/10.1186/1742-4690-3-50 Text en Copyright © 2006 Pumfery et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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	Pumfery, Anne de la Fuente, Cynthia Kashanchi, Fatah
spellingShingle	Pumfery, Anne de la Fuente, Cynthia Kashanchi, Fatah HTLV-1 Tax: centrosome amplification and cancer
author_facet	Pumfery, Anne de la Fuente, Cynthia Kashanchi, Fatah
author_sort	Pumfery, Anne
title	HTLV-1 Tax: centrosome amplification and cancer
title_short	HTLV-1 Tax: centrosome amplification and cancer
title_full	HTLV-1 Tax: centrosome amplification and cancer
title_fullStr	HTLV-1 Tax: centrosome amplification and cancer
title_full_unstemmed	HTLV-1 Tax: centrosome amplification and cancer
title_sort	htlv-1 tax: centrosome amplification and cancer
description	During interphase, each cell contains a single centrosome that acts as a microtubule organizing center for cellular functions in interphase and in mitosis. Centrosome amplification during the S phase of the cell cycle is a tightly regulated process to ensure that each daughter cell receives the proper complement of the genome. The controls that ensure that centrosomes are duplicated exactly once in the cell cycle are not well understood. In solid tumors and hematological malignancies, centrosome abnormalities resulting in aneuploidy is observed in the majority of cancers. These phenotypes are also observed in cancers induced by viruses, including adult T cell lymphoma which is caused by the human T cell lymphotrophic virus Type 1 (HTLV-1). Several reports have indicated that the HTLV-1 transactivator, Tax, is directly responsible for the centrosomal abnormalities observed in ATL cells. A recent paper in Nature Cell Biology by Ching et al. has shed some new light into how Tax may be inducing centrosome abnormalities. The authors demonstrated that 30% of ATL cells contained more than two centrosomes and expression of Tax alone induced supernumerary centrosomes. A cellular coiled-coil protein, Tax1BP2, was shown to interact with Tax and disruption of this interaction led to failure of Tax to induce centrosome amplification. Additionally, down-regulation of Tax1BP2 led to centrosome amplification. These results suggest that Tax1BP2 may be an important block to centrosome re-duplication that is observed in normal cells. Presently, a specific cellular protein that prevents centrosome re-duplication has not been identified. This paper has provided further insight into how Tax induces centrosome abnormalities that lead to ATL. Lastly, additional work on Tax1BP2 will also provide insight into how the cell suppresses centrosome re-duplication during the cell cycle and the role that Tax1BP2 plays in this important cellular pathway.
publisher	BioMed Central
publishDate	2006
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1555608/
_version_	1611387010006646784

HTLV-1 Tax: centrosome amplification and cancer

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