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星形胶质细胞上调基因-1的敲低抑制神经母细胞瘤细胞的增殖并增强对顺铂或阿霉素的化疗敏感性。

Knockdown of astrocyte elevated gene-1 inhibits proliferation and enhancing chemo-sensitivity to cisplatin or doxorubicin in neuroblastoma cells.

作者信息

Liu Haiyan, Song Xianrang, Liu Chunxi, Xie Li, Wei Ling, Sun Ruopeng

机构信息

Department of Pediatrics, Qilu Hospital of Shandong University, Jinan, PR China.

出版信息

J Exp Clin Cancer Res. 2009 Feb 15;28(1):19. doi: 10.1186/1756-9966-28-19.

DOI:10.1186/1756-9966-28-19
PMID:19216799
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2654547/
Abstract

BACKGROUND

Astrocyte elevated gene-1 (AEG-1) was originally characterized as a HIV-1-inducible gene in primary human fetal astrocyte. Recent studies highlight a potential role of AEG-1 in promoting tumor progression and metastasis. The aim of this study was to investigate if AEG-1 serves as a potential therapeutic target of human neuroblastoma.

METHODS

We employed RNA interference to reduce AEG-1 expression in human neuroblastoma cell lines and analyzed their phenotypic changes.

RESULTS

We found that the knockdown of AEG-1 expression in human neuroblastoma cells significantly inhibited cell proliferation and apoptosis. The specific downregulation induced cell arrest in the G0/G1 phase of cell cycle. In the present study, we also observed a significant enhancement of chemo-sensitivity to cisplatin and doxorubicin by knockdown of AEG-1.

CONCLUSION

Our study suggests that overexpressed AEG-1 enhance the tumorogenic properties of neuroblastoma cells. The inhibition of AEG-1 expression could be a new adjuvant therapy for neuroblastoma.

摘要

背景

星形胶质细胞上调基因1(AEG-1)最初被鉴定为原代人胎儿星形胶质细胞中一种HIV-1诱导基因。近期研究突出了AEG-1在促进肿瘤进展和转移方面的潜在作用。本研究的目的是调查AEG-1是否作为人类神经母细胞瘤的一个潜在治疗靶点。

方法

我们采用RNA干扰来降低人类神经母细胞瘤细胞系中AEG-1的表达,并分析其表型变化。

结果

我们发现,在人类神经母细胞瘤细胞中敲低AEG-1表达可显著抑制细胞增殖并诱导凋亡。特异性下调导致细胞周期停滞于G0/G1期。在本研究中,我们还观察到敲低AEG-1可显著增强对顺铂和阿霉素的化疗敏感性。

结论

我们的研究表明,过表达的AEG-1增强了神经母细胞瘤细胞的致瘤特性。抑制AEG-1表达可能成为神经母细胞瘤的一种新辅助治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f96d/2654547/9ba9ef9c1973/1756-9966-28-19-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f96d/2654547/3f013c8af3ab/1756-9966-28-19-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f96d/2654547/6dc114fdce87/1756-9966-28-19-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f96d/2654547/807f33901404/1756-9966-28-19-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f96d/2654547/9ba9ef9c1973/1756-9966-28-19-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f96d/2654547/3f013c8af3ab/1756-9966-28-19-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f96d/2654547/6dc114fdce87/1756-9966-28-19-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f96d/2654547/807f33901404/1756-9966-28-19-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f96d/2654547/9ba9ef9c1973/1756-9966-28-19-4.jpg

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