Additionally, the functions of miR-221/222 on glioblastoma cell angiogenesis were measured in vivo with microvessel density assayed. miR-221 and miR-222 were expressed at a high level and SOCS3 was at a low level in glioblastoma.
This study aims at validating microRNA-221 (miR-221) as a biomarker for glioblastoma, and understanding how miR-221 regulates glioblastoma progression.
In this study, we designed adenovirally-expressed shRNAs that functionally co-repressed the expression of miR-221 and miR-222, which are related to glioblastoma, to overcome the low efficiency of gene therapy.
In this work, we report that the ectopic modulation of NF-kB modifies miR-221/222 expression in prostate carcinoma and glioblastoma cell lines, where we had previously shown their oncogenic activity.
The up-regulation of miR-221 has been reported in carcinomas of the pancreas, breast, and papillary thyroid, as well as in glioblastoma and chronic lymphocytic leukaemia.
Global changes of mRNA expression reveals an increased activity of the interferon-induced signal transducer and activator of transcription (STAT) pathway by repression of miR-221/222 in glioblastoma U251 cells.
Antagonism of either microRNA 221 or 222 in glioblastoma cells also caused an increase in p27(Kip1) levels and enhanced expression of the luciferase reporter gene fused to the p27(Kip1) 3'UTR.
Antagonism of either microRNA 221 or 222 in glioblastoma cells also caused an increase in p27(Kip1) levels and enhanced expression of the luciferase reporter gene fused to the p27(Kip1) 3'UTR.
The most interesting results came from miR-221, strongly up-regulated in glioblastoma and from a set of brain-enriched miRNAs, miR-128, miR-181a, miR-181b, and miR-181c, which are down-regulated in glioblastoma.