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• W2604812571 abstract "Glioblastoma ( GBM ) is the most frequent and most malignant primary brain tumour in adults. GBM s have a unique landscape of somatic copy number alterations ( SCNA s), with the concomitant appearance of numerous driver amplifications and deletions. Here, we examined the genomic regions harbouring SCNA s and their impact on the GBM mi RN ome. We found that 40% of SCNA events covering 70–88% of the genomically altered regions, as identified by GISTIC and RAE algorithms, carried mi RNA genes. Of 1426 annotated mature mi RNA s analysed, ~ 14% ( n = 198) were mapped to such fragile loci. Further, we identified an intragenic mi RNA , miR‐4484 located on chromosome‐10, as a deleted and downregulated mi RNA in GBM . miR‐4484 exhibited a strong positive correlation with the expression of its host gene uroporphyrinogen III synthase ( UROS ), thereby indicating that the loss of miR‐4484 is a codeletion event in GBM. Overexpression of miR‐4484 reduced the colony‐forming ability and suppressed the migratory capacity of glioma cells. Analysis of the RNA ‐seq‐derived transcriptome upon exogenous miR‐4484 overexpression in conjunction with an integrative bioinformatics approach revealed several putative targets of miR‐4484. Unbiased functional enrichment of these targets through DAVID identified a cohort of important gene ontology terms, which possibly explain the functional role of miR‐4484 in gliomagenesis. Selected targets were validated and, importantly, were found to be upregulated in GBM . In brief, our study identified a panel of mi RNA s that are likely to be regulated by genomic deletions and amplifications. Further, miR‐4484 was found to be deleted and acts as a tumour suppressor mi RNA in GBM ." @default.
• W2604812571 created "2017-04-14" @default.
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• W2604812571 date "2017-05-24" @default.
• W2604812571 modified "2023-10-04" @default.
• W2604812571 title "Impact of somatic copy number alterations on the glioblastoma miRNome: miR-4484 is a genomically deleted tumour suppressor" @default.
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• W2604812571 doi "https://doi.org/10.1002/1878-0261.12060" @default.
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