====== MicroRNA ====== MicroRNAs ([[miRNA]]s) are small, non-coding [[RNA molecule]]s, typically about 20-25 nucleotides long, that play a crucial role in regulating [[gene expression]]. They function by binding to complementary sequences in messenger RNA ([[mRNA]]) molecules, leading to the degradation of the mRNA or the inhibition of its translation into proteins. They play essential roles in post-transcriptional [[gene regulation]]. They are involved in various biological processes, including [[cell]] [[development]], [[differentiation]], [[proliferation]], [[apoptosis]], and response to environmental cues. More and more [[evidence]] shows that [[microRNA]]s (MicroRNAs) play an important role in the diagnosis and prognosis of human diseases. ---- MicroRNAs (miRs) act as oncogenes or tumor-suppressor genes and regulate the proliferation, apoptosis, invasion, differentiation, angiogenesis, and behavior of [[glioma stem cell]]s, which are important in [[glioma recurrence]] and development. ---- ===== Key Features of MicroRNAs ===== ==== Biogenesis ==== miRNAs are transcribed from DNA and initially exist as longer primary transcripts (pri-miRNAs). They undergo several processing steps involving enzymes like Drosha and Dicer to become mature miRNAs. Mechanism of Action: Once processed, miRNAs are incorporated into the RNA-induced silencing complex (RISC). The RISC then uses the miRNA as a guide to bind to target mRNAs based on sequence complementarity. ==== Regulation of Gene Expression ==== miRNAs can regulate multiple target genes, influencing various biological processes such as development, cell differentiation, proliferation, and apoptosis. They can act as tumor suppressors or oncogenes depending on the context. ==== Role in Diseases ==== Dysregulation of miRNAs has been implicated in various diseases, including cancer, cardiovascular diseases, and neurological disorders. They are being explored as potential biomarkers for disease diagnosis and as therapeutic targets. Research and Therapeutics: miRNA-based therapies are being developed, including miRNA mimics and inhibitors (antagomiRs) to restore normal function in diseased states. ===== MicroRNA in Neurosurgery ===== [[MicroRNA in Neurosurgery]]. ===== Types ===== [[miR 9]] [[miR 16]] [[miR 19a]] [[miR 21]] [[miR 22]] [[miR 24]] [[miR 25]]-5p [[miR 26a]] [[miR 26b]] [[miR 29a]] [[miR 34]] [[miR 105]] [[miR 126]] [[miR 128]] [[miR 130b]] [[miR 132]] [[miR 144]] [[miR 145]] [[miR 148]] [[miR 151]] [[miR 152]] [[miR 155]] [[miR 181c]] [[miR 181d]] [[miR 182]] [[miR 199]] [[miR 200]] [[miR 203]] [[miR 205]] [[miR 206]] [[miR 210]] [[miR 215]] [[miR 218]] [[miR 221]] [[miR 302a]] [[miR 328]] [[miR 351]] [[miR 361-5p]] [[miR 375]] [[miR 378]] [[miR 431]] [[miR 433]] [[miR 448]] [[miR 489]] [[miR 494]] [[miR 497]] [[miR 588]] [[miR 613]] [[miR 720]] [[miR 942]] [[miR 944]] [[miR 1118]] [[miR 1297]] ..... Jiang et al., found a positive correlation between the levels of miR-127-3p and the cell migration and invasion abilities in several human Glioblastoma cell lines. Theyshowed that miR-127-3p promoted cell migration and invasion of Glioblastoma cells using in vitro cell lines and in vivo mouse models. They identified SEPT7, a known tumor-suppressor gene that has been reported to suppress Glioblastoma cell migration and invasion, as a direct target of miR-127-3p. SEPT7 was able to partially abrogate the effect of miR-127-3p on cell migration and invasion. In addition, microarray analysis revealed that miR-127-3p regulated a number of migration and invasion-related genes. Finally, they verified that miR-127-3p affected the remodeling of the actin cytoskeleton mediated by SEPT7 in Glioblastoma cells ((Jiang H, Hua D, Zhang J, Lan Q, Huang Q, Yoon JG, Han X, Li L, Foltz G, Zheng S, Lin B. MicroRNA-127-3p promotes glioblastoma cell migration and invasion by targeting the tumor-suppressor gene SEPT7. Oncol Rep. 2014 Mar 5. doi: 10.3892/or.2014.3055. [Epub ahead of print] PubMed PMID: 24604520.)). MiR-132, miR-15a and miR-16 have been implicated in the pathogenesis of many types of cancer, including pituitary tumors. However, the molecular mechanism of these MicroRNAs in pituitary tumor growth and metastases is still unclear. Here, we showed that miR-132 and miR-15a/16 were less expressed in pituitary tumor cell lines, as well as in invasive pituitary tumor tissues, compared to non-invasive tumor tissues. We described that overexpression of miR-132 and miR-15a/16 resulted in the suppression of pituitary tumor cell proliferation, migration and invasion, respectively, and also inhibits the expression of proteins involved in Epithelial to Mesenchymal Transition (EMT). Then, we show that these MicroRNAs synergistically target Sox5 in pituitary tumor. Moreover, we found that Sox5 overexpression partially rescued miR-132, miR-15a and miR-16-mediated inhibition of cell migration, invasion and cell growth. Finally, we confirmed that Sox5 was upregulated in invasive pituitary tumor tissues, compared to non-invasion tissues. In conclusion, our data indicate that miR-132 and miR-15a/16 act as tumor suppressor genes in pituitary tumor by directly targetting Sox5, and imply that these MicroRNAs have potential as therapeutic targets for invasive pituitary tumor ((Renjie W, Haiqian L. MiR-132, miR-15a and miR-16 synergistically inhibit pituitary tumor cell proliferation, invasion and migration by targeting Sox5. Cancer Lett. 2015 Jan 28;356(2 Pt B):568-78. doi: 10.1016/j.canlet.2014.10.003. Epub 2014 Oct 8. PubMed PMID: 25305447. )). ====MicroRNA and aneurysm==== Results support that dysregulated microRNAs may have a pathogenic role in [[intracranial aneurysm]]s. Disruption of the protein translation process may have a pathogenic role in the development of intracranial aneurysms ((Liu D, Han L, Wu X, Yang X, Zhang Q, Jiang F. Genome-wide microRNA changes in human intracranial aneurysms. BMC Neurol. 2014 Oct 10;14:188. doi: 10.1186/s12883-014-0188-x. PubMed PMID: 25300531; PubMed Central PMCID: PMC4210474. )). The molecular mechanisms behind [[intracranial aneurysm]] formation and rupture remain poorly understood. The MicroRNA and mRNA interactions and expression levels in cerebral aneurysm tissue from human subjects were profiled. A prospective case-control study was performed on human subjects to characterize the differential expression of mRNA and MicroRNA in unruptured cerebral aneurysms in comparison with control tissue (healthy superficial temporal arteries [STA]). Ion Torrent was used for deep RNA sequencing. Affymetrix MicroRNA microarrays were used to analyze MicroRNA expression, whereas NanoString nCounter technology was used for validation of the identified targets. Overall, 7 [[unruptured intracranial aneurysm]] and 10 STA specimens were collected. Several differentially expressed genes were identified in aneurysm tissue, with MMP-13 (fold change 7.21) and various collagen genes (COL1A1, COL5A1, COL5A2) being among the most upregulated. In addition, multiple MicroRNAs were significantly differentially expressed, with miR-21 (fold change 16.97) being the most upregulated, and miR-143-5p (fold change -11.14) being the most downregulated. From these, miR-21, miR-143, and miR-145 had several significantly anticorrelated target genes in the cohort that are associated with smooth muscle cell function, extracellular matrix remodeling, inflammation signaling, and lipid accumulation. All these processes are crucial to the pathophysiology of cerebral aneurysms. This analysis identified differentially expressed genes and MicroRNAs in unruptured human cerebral aneurysms, suggesting the possibility of a role for MicroRNAs in aneurysm formation. Further investigation for their importance as therapeutic targets is needed ((Bekelis K, Kerley-Hamilton JS, Teegarden A, Tomlinson CR, Kuintzle R, Simmons N, Singer RJ, Roberts DW, Kellis M, Hendrix DA. MicroRNA and gene expression changes in unruptured human cerebral aneurysms. J Neurosurg. 2016 Dec;125(6):1390-1399. PubMed PMID: 26918470; PubMed Central PMCID: PMC5001931. )). ====MicroRNA and mesial temporal lobe epilepsy==== A total of 50 [[microRNA]]s were found to be differentially expressed in [[mesial temporal lobe epilepsy]] with [[hippocampal sclerosis]] (mTLE-HS) compared with healthy controls. Among them, 2 were increased and 48 were decreased. The 6 significant differentially expressed candidate microRNAs (miR-3613-5p, miR-4668-5p, miR-8071, miR-197-5p, miR-4322, and miR-6781-5p ) in exosome were validated. The bioinformatics analysis showed that the potential target genes of these microRNAs were involved in biological processes, molecular functions, and cellular components. Similarly, these microRNAs also affected axon guidance, pathways in cancer, regulation of the actin cytoskeleton, focal adhesion, the calcium signaling pathway, the MAPK signaling pathway, and the PI3K-Akt signaling pathway. Among 6 candidate microRNAs, miR-8071 had the best diagnostic value for mTLE-HS with 83.33% sensitivity and 96.67% specificity, and was associated with seizure severity. This study indicated that exosomal microRNAs, may be regulators for the seizure development in mTLE-HS, and can be used as potential therapeutic targets and biomarker for diagnosis in mTLE-HS ((Yan S, Zhang H, Xie W, Meng F, Zhang K, Jiang Y, Zhang X, Zhang J. Altered microRNA profiles in plasma exosomes from mesial temporal lobe epilepsy with hippocampal sclerosis. Oncotarget. 2016 Dec 1. doi: 10.18632/oncotarget.13744. [Epub ahead of print] PubMed PMID: 27926529. )). ===== References =====