Abstract
BackgroundAstrocyte 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.MethodsWe employed RNA interference to reduce AEG-1 expression in human neuroblastoma cell lines and analyzed their phenotypic changes.ResultsWe 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.ConclusionOur 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.
Highlights
Astrocyte elevated gene-1 (AEG-1) was originally characterized as a human immunodeficiency virus (HIV)-1-inducible gene in primary human fetal astrocyte
Knock-down of AEG-1 by specific siRNAs In order to knock down AEG-1, we used two different 21base pair siRNA constructs: AEG-1-siRNA1 and AEG-1siRNA2
AEG-1 knockdown inhibits proliferation and promotes apoptosis in neuroblastoma cells In order to examine the role of AEG-1 on neuroblastoma cell proliferation, we examined the effect of AEG-1 siRNA on neuroblastoma cell growth and colonogenic assay
Summary
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. It is thought to arise from the anomalous arrest of multi-potential embryonal cells of neural crest origin during differentiation. Prognosis of neuroblastoma is in part related to tumor stage, the presence or absence of N-myc amplification, nuclear ploidy and the age of onset [2,3,4]. Complete or partial remissions are achieved in 74% of these children with multi-agent high-dose therapy, long-term survivors represent only 15–20% of relapsed patients [5,6]. New approaches to inhibit aggressiveness and increase chemo-sensitivity of neuroblastoma to anticancer agents are required
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