Abstract
Aberrant expression of microRNAs hae been shown to be closely associated with glioblastoma cell proliferation, apoptosis and drug resistance. However, mechanisms underlying the role of mcroRNAs in glioblastoma cell growth and apoptosis are not fully understood. In this study, we report that miR-503 is overexpressed in glioblastoma tissue compared with normal human brain tissue. Mechanistically, miR-503 can be induced by TGF-β1 at the transcriptional level by binding the smad2/3 binding elements in the promoter. Ectopic overexpression of miR-503 promotes cell growth and inhibits apoptosis by targeting PDCD4. In contrast, inhibition of miR-503 reduces cell growth. Furthermore, miR-503 inhibitor augments the growth inhibitory effect of temozolomide in glioblastoma cells. These results establish miR-503 as a promising molecular target for glioblastoma therapy.
Highlights
Aberrant expression of microRNAs hae been shown to be closely associated with glioblastoma cell proliferation, apoptosis and drug resistance
We found that miR-503 is overexpressed in human glioblastoma tissues compared with normal brain tissues, and that TGF-β1 can induce miR-503 expression at the transcriptional level by binding the promoter
The result showed that miR-503 is significantly upregulated in glioblastoma tissue compared with normal brain tissue (p < 0.001) (Fig. 1A)
Summary
Aberrant expression of microRNAs hae been shown to be closely associated with glioblastoma cell proliferation, apoptosis and drug resistance. We report that miR-503 is overexpressed in glioblastoma tissue compared with normal human brain tissue. Ectopic overexpression of miR-503 promotes cell growth and inhibits apoptosis by targeting PDCD4. The aberrant expression of many microRNAs has been reported to be associated with progression of various cancers. MicroRNA-503 was found to be upregulated in esophageal cancer tissues compared to adjacent normal tissues and to promote tumor progression[10]. We found that miR-503 is overexpressed in human glioblastoma tissues compared with normal brain tissues, and that TGF-β1 can induce miR-503 expression at the transcriptional level by binding the promoter. These results establish miR-503 as a promising molecular target for glioblastoma therapy
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