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成人T细胞白血病细胞系中CD30表达升高：在组成性核因子-κB激活中的可能作用

Elevated expression of CD30 in adult T-cell leukemia cell lines: possible role in constitutive NF-kappaB activation.

作者信息

Higuchi Masaya, Matsuda Takehiro, Mori Naoki, Yamada Yasuaki, Horie Ryouichi, Watanabe Toshiki, Takahashi Masahiko, Oie Masayasu, Fujii Masahiro

机构信息

Division of Virology, Niigata University Graduate School of Medical and Dental Sciences, Niigata 951-8510, Japan.

出版信息

Retrovirology. 2005 May 6;2:29. doi: 10.1186/1742-4690-2-29.

DOI:10.1186/1742-4690-2-29
PMID:15876358
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1274245/
Abstract

BACKGROUND

Human T-cell leukemia virus type 1 (HTLV-1) is associated with the development of adult T-cell leukemia (ATL). HTLV-1 encoded Tax1 oncoprotein activates the transcription of genes involved in cell growth and anti-apoptosis through the NF-kappaB pathway, and is thought to play a critical role in the pathogenesis of ATL. While Tax1 expression is usually lost or minimal in ATL cells, these cells still show high constitutive NF-kappaB activity, indicating that genetic or epigenetic changes in ATL cells induce activation independent of Tax1. The aim of this study was to identify the molecules responsible for the constitutive activation of NF-kappaB in ATL cells using a retroviral functional cloning strategy.

RESULTS

Using enhanced green fluorescent protein (EGFP) expression and blasticidin-resistance as selection markers, several retroviral cDNA clones exhibiting constitutive NF-kappaB activity in Rat-1 cells, including full-length CD30, were obtained from an ATL cell line. Exogenous stable expression of CD30 in Rat-1 cells constitutively activated NF-kappaB. Elevated expression of CD30 was identified in all ATL lines examined, and primary ATL cells from a small number of patients (8 out of 66 cases).

CONCLUSION

Elevated CD30 expression is considered one of the causes of constitutive NF-kappaB activation in ATL cells, and may be involved in ATL development.

摘要

背景

人类1型T细胞白血病病毒（HTLV-1）与成人T细胞白血病（ATL）的发生有关。HTLV-1编码的Tax1癌蛋白通过NF-κB途径激活参与细胞生长和抗凋亡的基因转录，被认为在ATL的发病机制中起关键作用。虽然Tax1在ATL细胞中的表达通常缺失或极低，但这些细胞仍表现出较高的组成性NF-κB活性，这表明ATL细胞中的遗传或表观遗传变化可诱导不依赖Tax1的激活。本研究的目的是使用逆转录病毒功能克隆策略鉴定负责ATL细胞中NF-κB组成性激活的分子。

结果

以增强型绿色荧光蛋白（EGFP）表达和杀稻瘟菌素抗性作为选择标记，从一株ATL细胞系中获得了几个在大鼠-1细胞中表现出组成性NF-κB活性的逆转录病毒cDNA克隆，包括全长CD30。大鼠-1细胞中CD30的外源性稳定表达可组成性激活NF-κB。在所检测的所有ATL细胞系以及少数患者（66例中的8例）的原发性ATL细胞中均鉴定出CD30表达升高。

结论

CD30表达升高被认为是ATL细胞中组成性NF-κB激活的原因之一，可能参与了ATL的发生发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b3f/1274245/4c0ac6699d33/1742-4690-2-29-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b3f/1274245/1975e166fbb2/1742-4690-2-29-1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b3f/1274245/4c0ac6699d33/1742-4690-2-29-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b3f/1274245/1975e166fbb2/1742-4690-2-29-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b3f/1274245/44792b4b9a2d/1742-4690-2-29-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b3f/1274245/532f06b1ced2/1742-4690-2-29-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b3f/1274245/2ef9d8f157cd/1742-4690-2-29-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b3f/1274245/4c0ac6699d33/1742-4690-2-29-5.jpg

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