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Overexpression of miR-506 suppresses proliferation and promotes apoptosis of osteosarcoma cells by targeting astrocyte elevated gene-1

View Article: PubMed Central - PubMed

ABSTRACT

There is increasing evidence that microRNAs (miRs) are implicated in tumor development and progression; however, their specific roles in osteosarcoma are not well understood. The aim of the present study was to investigate the role of miR-506 in the pathogenesis of osteosarcoma. The expression levels of miR-506 and astrocyte elevated gene-1 (AEG-1) mRNA were detected using quantitative polymerase chain reaction, and the protein levels of AEG-1, β-catenin, c-myc and cyclin D1 were determined using western blot analysis. The effects of miR-506 and AEG-1 on cell viability, colony forming ability and apoptosis were assessed using MTT assay, colony formation assay, and flow cytometry, respectively. Lucifer reporter assays were used to demonstrate whether AEG-1 is a direct target of miR-506. The present study identified that miR-506 was downregulated in osteosarcoma tissues and cells. Overexpression of miR-506 suppressed the proliferation and induced apoptosis in osteosarcoma cells in vitro and inhibited tumor formation in vivo. Overexpression of miR-506 significantly inhibited the luciferase activity of AEG-1 with a wild-type 3′-untranslated region, providing clear evidence that AEG-1 was a direct and functional downstream target of miR-506. Similar to the overexpression of miR-506, downregulation of AEG-1 lead to an inhibitory effect on osteosarcoma in vitro. Furthermore, overexpression of miR-506 or downregulation of AEG-1 inhibited the Wnt/β-catenin signaling pathway, and inhibition of this pathway by β-catenin small interfering RNA or CGP049090, a small molecule inhibitor, suppressed cell proliferation and induced apoptosis in vitro. Overall, the present data indicated that miR-506 functions as a tumor suppressor by targeting AEG-1 in osteosarcoma via the regulation of the Wnt/β-catenin signaling pathway.

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Effects of miR-506 and AEG-1 on the apoptosis of human osteosarcoma MG63 cells. (A) Overexpression of miR-506 enhanced the apoptosis of MG63 cells. *P<0.05 vs. miR-control. (B) Knockdown of AEG-1 induced the apoptosis of MG63 cells. *P<0.05 vs. si-control. miR, microRNA; AEG-1, astrocyte elevated gene-1; si, small interfering RNA.
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f3-ol-0-0-4827: Effects of miR-506 and AEG-1 on the apoptosis of human osteosarcoma MG63 cells. (A) Overexpression of miR-506 enhanced the apoptosis of MG63 cells. *P<0.05 vs. miR-control. (B) Knockdown of AEG-1 induced the apoptosis of MG63 cells. *P<0.05 vs. si-control. miR, microRNA; AEG-1, astrocyte elevated gene-1; si, small interfering RNA.

Mentions: The present study additionally assessed the effects of miR-506 and AEG-1 on the apoptosis of MG63 cells. Overexpression of miR-506 significantly increased the apoptotic rate of MG63 cells compared to the miR-control-transfected group (P=0.0265; Fig. 3A). Similarly, downregulation of AEG-1 induced a higher apoptotic rate of MG63 cells compared with the si-control group (P=0.0137; Fig. 3B). Overall, these results indicate that overexpression of miR-506 and downregulation of AEG-1 have a clear ability to induce MG63 cell apoptosis.


Overexpression of miR-506 suppresses proliferation and promotes apoptosis of osteosarcoma cells by targeting astrocyte elevated gene-1
Effects of miR-506 and AEG-1 on the apoptosis of human osteosarcoma MG63 cells. (A) Overexpression of miR-506 enhanced the apoptosis of MG63 cells. *P<0.05 vs. miR-control. (B) Knockdown of AEG-1 induced the apoptosis of MG63 cells. *P<0.05 vs. si-control. miR, microRNA; AEG-1, astrocyte elevated gene-1; si, small interfering RNA.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4998420&req=5

f3-ol-0-0-4827: Effects of miR-506 and AEG-1 on the apoptosis of human osteosarcoma MG63 cells. (A) Overexpression of miR-506 enhanced the apoptosis of MG63 cells. *P<0.05 vs. miR-control. (B) Knockdown of AEG-1 induced the apoptosis of MG63 cells. *P<0.05 vs. si-control. miR, microRNA; AEG-1, astrocyte elevated gene-1; si, small interfering RNA.
Mentions: The present study additionally assessed the effects of miR-506 and AEG-1 on the apoptosis of MG63 cells. Overexpression of miR-506 significantly increased the apoptotic rate of MG63 cells compared to the miR-control-transfected group (P=0.0265; Fig. 3A). Similarly, downregulation of AEG-1 induced a higher apoptotic rate of MG63 cells compared with the si-control group (P=0.0137; Fig. 3B). Overall, these results indicate that overexpression of miR-506 and downregulation of AEG-1 have a clear ability to induce MG63 cell apoptosis.

View Article: PubMed Central - PubMed

ABSTRACT

There is increasing evidence that microRNAs (miRs) are implicated in tumor development and progression; however, their specific roles in osteosarcoma are not well understood. The aim of the present study was to investigate the role of miR-506 in the pathogenesis of osteosarcoma. The expression levels of miR-506 and astrocyte elevated gene-1 (AEG-1) mRNA were detected using quantitative polymerase chain reaction, and the protein levels of AEG-1, &beta;-catenin, c-myc and cyclin D1 were determined using western blot analysis. The effects of miR-506 and AEG-1 on cell viability, colony forming ability and apoptosis were assessed using MTT assay, colony formation assay, and flow cytometry, respectively. Lucifer reporter assays were used to demonstrate whether AEG-1 is a direct target of miR-506. The present study identified that miR-506 was downregulated in osteosarcoma tissues and cells. Overexpression of miR-506 suppressed the proliferation and induced apoptosis in osteosarcoma cells in vitro and inhibited tumor formation in vivo. Overexpression of miR-506 significantly inhibited the luciferase activity of AEG-1 with a wild-type 3&prime;-untranslated region, providing clear evidence that AEG-1 was a direct and functional downstream target of miR-506. Similar to the overexpression of miR-506, downregulation of AEG-1 lead to an inhibitory effect on osteosarcoma in vitro. Furthermore, overexpression of miR-506 or downregulation of AEG-1 inhibited the Wnt/&beta;-catenin signaling pathway, and inhibition of this pathway by &beta;-catenin small interfering RNA or CGP049090, a small molecule inhibitor, suppressed cell proliferation and induced apoptosis in vitro. Overall, the present data indicated that miR-506 functions as a tumor suppressor by targeting AEG-1 in osteosarcoma via the regulation of the Wnt/&beta;-catenin signaling pathway.

No MeSH data available.


Related in: MedlinePlus