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

Liu H, Song X, Liu C, Xie L, Wei L, Sun R - J. Exp. Clin. Cancer Res. (2009)

Bottom Line: 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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Pediatrics, Qilu Hospital of Shandong University, Jinan, PR China. liuhaiyan26@yahoo.com.cn

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.

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Related in: MedlinePlus

Knock-down of AEG-1 by specific siRNAs. Fourty-eight hours after transfection, cells were harvested. (A), AEG-1 mRNA levels were quantified by real-time PCR analysis. Data were normalized by using GAPDH as an internal standard. *P < 0.05 vs. parental cells. (B, C) AEG-1 protein level was analyzed by western blot. β-actin expression was monitored as the internal standard. *P < 0.05 vs. parental cells. These experiments were performed in triplicate.
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Figure 1: Knock-down of AEG-1 by specific siRNAs. Fourty-eight hours after transfection, cells were harvested. (A), AEG-1 mRNA levels were quantified by real-time PCR analysis. Data were normalized by using GAPDH as an internal standard. *P < 0.05 vs. parental cells. (B, C) AEG-1 protein level was analyzed by western blot. β-actin expression was monitored as the internal standard. *P < 0.05 vs. parental cells. These experiments were performed in triplicate.

Mentions: In order to knock down AEG-1, we used two different 21-base pair siRNA constructs: AEG-1-siRNA1 and AEG-1-siRNA2. As shown in Figure 1, transfected M17 and SK-N-SH with either AEG-1-siRNA1 or AEG-1-siRNA2 resulted in knock down of AEG-1 at both the transcription and translation levels in each neuroblastoma cell lines. Control siRNA transfected cells had no significant impact on AEG-1 expression levels compared with parental cells. AEG-1-siRNA1 was used to process the follow investigation.


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

Liu H, Song X, Liu C, Xie L, Wei L, Sun R - J. Exp. Clin. Cancer Res. (2009)

Knock-down of AEG-1 by specific siRNAs. Fourty-eight hours after transfection, cells were harvested. (A), AEG-1 mRNA levels were quantified by real-time PCR analysis. Data were normalized by using GAPDH as an internal standard. *P < 0.05 vs. parental cells. (B, C) AEG-1 protein level was analyzed by western blot. β-actin expression was monitored as the internal standard. *P < 0.05 vs. parental cells. These experiments were performed in triplicate.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2654547&req=5

Figure 1: Knock-down of AEG-1 by specific siRNAs. Fourty-eight hours after transfection, cells were harvested. (A), AEG-1 mRNA levels were quantified by real-time PCR analysis. Data were normalized by using GAPDH as an internal standard. *P < 0.05 vs. parental cells. (B, C) AEG-1 protein level was analyzed by western blot. β-actin expression was monitored as the internal standard. *P < 0.05 vs. parental cells. These experiments were performed in triplicate.
Mentions: In order to knock down AEG-1, we used two different 21-base pair siRNA constructs: AEG-1-siRNA1 and AEG-1-siRNA2. As shown in Figure 1, transfected M17 and SK-N-SH with either AEG-1-siRNA1 or AEG-1-siRNA2 resulted in knock down of AEG-1 at both the transcription and translation levels in each neuroblastoma cell lines. Control siRNA transfected cells had no significant impact on AEG-1 expression levels compared with parental cells. AEG-1-siRNA1 was used to process the follow investigation.

Bottom Line: 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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Pediatrics, Qilu Hospital of Shandong University, Jinan, PR China. liuhaiyan26@yahoo.com.cn

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.

Show MeSH
Related in: MedlinePlus