Abstract
Glioblastoma (GBM), a grade IV brain tumor, is known for its heterogenicity and its resistance to the current treatment regimen. Over the last few decades, a significant amount of new molecular and genetic findings has been reported regarding factors contributing to GBM’s development into a lethal phenotype and its overall poor prognosis. MicroRNA (miRNAs) are small non-coding sequences of RNA that regulate and influence the expression of multiple genes. Many research findings have highlighted the importance of miRNAs in facilitating and controlling normal biological functions, including cell differentiation, proliferation, and apoptosis. Furthermore, miRNAs’ ability to initiate and promote cancer development, directly or indirectly, has been shown in many types of cancer. There is a clear association between alteration in miRNAs expression in GBM’s ability to escape apoptosis, proliferation, and resistance to treatment. Further, miRNAs regulate the already altered pathways in GBM, including P53, RB, and PI3K-AKT pathways. Furthermore, miRNAs also contribute to autophagy at multiple stages. In this review, we summarize the functions of miRNAs in GBM pathways linked to dysregulation of cell cycle control, apoptosis and resistance to treatment, and the possible use of miRNAs in clinical settings as treatment and prediction biomarkers.
Highlights
Glioblastoma (GBM) is a grade IV tumor, which develops from the brain’s supporting glia cells and represents around 70–75% of total glioma cases [1]
Gene profiling of GBM reveals a number of genes to be highly dysregulated, including Protein 53 (P53), phosphatase and tensin homolog (PTEN), retinoblastoma RB, survivine (BIRC5), and O6-methylguanine-DNA methyltransferase (MGMT) [9]
Amplification of the epidermal growth factor receptor (EGFR) impacts pathways linked to cell death [10]
Summary
Glioblastoma (GBM) is a grade IV tumor, which develops from the brain’s supporting glia cells and represents around 70–75% of total glioma cases [1]. Secondary GBM is less common and progresses from pre-existing anaplastic astrocytoma or lowgrade diffuse astrocytoma [4–6] Both primary and secondary GBMs display alteration in tumor Protein 53 (P53) pathway (87%), receptor tyrosine kinase pathway (RTK) (88%), and retinoblastoma pathway (78%) [7]. MiRNAs are regulated by their transcription units; any dysregulation of these units can lead to deregulation of their gene expression levels, a single unit can activate or deactivate many of its miRNA target genes [19]. These facts make miRNA an exciting factor to look at its possible function in healthy biological status and in malignancies
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