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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

AEG-1 knockdown inhibits proliferation and promotes apoptosis in neuroblastoma cells. (A, B) Cell viability was evaluated by MTT assay. The results of cell proliferation assay showed a significant decrease in the number of cells by 42.9% in M17 and 49.5% in SK-N-SH in 72 h. (C, D) Compared with that seen in the parental cells, the number of colonies was significantly reduced in the AEG-1 siRNA1 transfected group (*P < 0.05 vs. parental cells). Each experiment was performed three times in triplicate. (E) The apoptosis rate of AEG-1 siRNA1 transfected cells significantly increased by 9.6% ± 1.7% in M17 and 9.0% ± 1.4% in SK-N-SH cells (*P < 0.05 vs. parental cells), respectively. (F) Representative results are shown. These experiments were performed in triplicate.
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Figure 2: AEG-1 knockdown inhibits proliferation and promotes apoptosis in neuroblastoma cells. (A, B) Cell viability was evaluated by MTT assay. The results of cell proliferation assay showed a significant decrease in the number of cells by 42.9% in M17 and 49.5% in SK-N-SH in 72 h. (C, D) Compared with that seen in the parental cells, the number of colonies was significantly reduced in the AEG-1 siRNA1 transfected group (*P < 0.05 vs. parental cells). Each experiment was performed three times in triplicate. (E) The apoptosis rate of AEG-1 siRNA1 transfected cells significantly increased by 9.6% ± 1.7% in M17 and 9.0% ± 1.4% in SK-N-SH cells (*P < 0.05 vs. parental cells), respectively. (F) Representative results are shown. These experiments were performed in triplicate.

Mentions: 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. As shown in Figure 2A and 2B, AEG-1-siRNA1 significantly decreases cell proliferation by 42.9% in M17 and 49.5% in SK-N-SH at 72 hours compared to control group, respectively. Furthermore, colony forming ability was also affected by transfection with AEG-1 siRNA1 (Figure 2C and 2D).


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)

AEG-1 knockdown inhibits proliferation and promotes apoptosis in neuroblastoma cells. (A, B) Cell viability was evaluated by MTT assay. The results of cell proliferation assay showed a significant decrease in the number of cells by 42.9% in M17 and 49.5% in SK-N-SH in 72 h. (C, D) Compared with that seen in the parental cells, the number of colonies was significantly reduced in the AEG-1 siRNA1 transfected group (*P < 0.05 vs. parental cells). Each experiment was performed three times in triplicate. (E) The apoptosis rate of AEG-1 siRNA1 transfected cells significantly increased by 9.6% ± 1.7% in M17 and 9.0% ± 1.4% in SK-N-SH cells (*P < 0.05 vs. parental cells), respectively. (F) Representative results are shown. 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 2: AEG-1 knockdown inhibits proliferation and promotes apoptosis in neuroblastoma cells. (A, B) Cell viability was evaluated by MTT assay. The results of cell proliferation assay showed a significant decrease in the number of cells by 42.9% in M17 and 49.5% in SK-N-SH in 72 h. (C, D) Compared with that seen in the parental cells, the number of colonies was significantly reduced in the AEG-1 siRNA1 transfected group (*P < 0.05 vs. parental cells). Each experiment was performed three times in triplicate. (E) The apoptosis rate of AEG-1 siRNA1 transfected cells significantly increased by 9.6% ± 1.7% in M17 and 9.0% ± 1.4% in SK-N-SH cells (*P < 0.05 vs. parental cells), respectively. (F) Representative results are shown. These experiments were performed in triplicate.
Mentions: 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. As shown in Figure 2A and 2B, AEG-1-siRNA1 significantly decreases cell proliferation by 42.9% in M17 and 49.5% in SK-N-SH at 72 hours compared to control group, respectively. Furthermore, colony forming ability was also affected by transfection with AEG-1 siRNA1 (Figure 2C and 2D).

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