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人垂体肿瘤转化基因与人类1型T细胞白血病病毒Tax蛋白协同转化活性的证据。

Evidence for cooperative transforming activity of the human pituitary tumor transforming gene and human T-cell leukemia virus type 1 Tax.

作者信息

Sheleg Sergey V, Peloponese Jean-Marie, Chi Ya-Hui, Li Yan, Eckhaus Michael, Jeang Kuan-Teh

机构信息

Molecular Virology Section, Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.

出版信息

J Virol. 2007 Aug;81(15):7894-901. doi: 10.1128/JVI.00555-07. Epub 2007 May 16.

DOI:10.1128/JVI.00555-07
PMID:17507465
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1951308/
Abstract

Aneuploidy is frequent in cancers. Recently it was found that pituitary tumor transforming gene (PTTG; also called Pds1p or securin) is overexpressed in many different tumors. Human T-cell leukemia virus type 1 (HTLV-1) is a retrovirus that primarily infects CD4+ T lymphocytes and causes adult T-cell leukemia. Here, we report that overexpression of human PTTG cooperated with the HTLV-I Tax oncoprotein in cellular transformation. Coexpression of Tax and PTTG enhanced chromosomal instability and neoplastic changes to levels greater than overexpression of either factor singularly. Cells that overexpressed both PTTG and Tax induced tumors more robustly in nude mice than cells that expressed either PTTG alone or Tax alone.

摘要

非整倍体在癌症中很常见。最近发现垂体肿瘤转化基因(PTTG;也称为Pds1p或分离酶)在许多不同肿瘤中过度表达。1型人类T细胞白血病病毒(HTLV-1)是一种逆转录病毒,主要感染CD4+T淋巴细胞并导致成人T细胞白血病。在此,我们报告人类PTTG的过度表达与HTLV-I Tax癌蛋白在细胞转化中协同作用。Tax和PTTG的共表达增强了染色体不稳定性和肿瘤性变化,其程度大于单独过度表达任何一种因子。同时过度表达PTTG和Tax的细胞在裸鼠中比单独表达PTTG或Tax的细胞更有力地诱导肿瘤形成。

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本文引用的文献

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Aberrant accumulation of PTTG1 induced by a mutated thyroid hormone beta receptor inhibits mitotic progression.由突变的甲状腺激素β受体诱导的PTTG1异常积累会抑制有丝分裂进程。
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The retroviral oncoprotein Tax targets the coiled-coil centrosomal protein TAX1BP2 to induce centrosome overduplication.逆转录病毒癌蛋白Tax靶向卷曲螺旋中心体蛋白TAX1BP2以诱导中心体过度复制。
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