Page 2 Hines, Marcum, Strong, Wade • Differential MicroRNA Expression radio resistance (Gimple et al., 2019). As a key component in glioblastoma’s resistance to modern therapies, miRNAs are ideal targets for the progression of glioblastoma treatment effectiveness. MicroRNA in Other Cancers Besides being found in glioblastoma, microRNA (miRNA) also has a distinct role in other cancers. MicroRNA is the key to knowing how cancer stem cells (CSCs), specifically neural CSCs, are created and can ultimately be destroyed because of how CSCs downregulate pro-apoptotic miRNA as compared to normal neural stem cells (NSCs) (Diana et al., 2020). This allows for unregulated growth of the cancerous cells and leads to a multitude of possible cancers. When restored, these pro-apoptotic miRNAs could inhibit anti-apoptotic genes allowing them to act as tumor suppressant miRNAs (Diana et al., 2020). This kind of information is important to treat multiple different neural cancers. CSCs avoid apoptosis and are nearly immune to most regular forms of treatment (Diana et al., 2020). Neural CSCs can escape apoptosis by the downregulation of miRNAs and avoid other treatments by downregulation of death receptors or anti-apoptotic factors. CSCs including brain tumor stem cells, glioma stem cells, medulloblastoma, neuroblastoma, and melanoma stem cells are the cause of multiple different cancers. (Diana et al., 2020). Although other cancers use miRNAs, the focus in research has been on the neurological side. MicroRNA and Autoimmune Diseases MicroRNA plays an important role in the development or regulation of cancer, but recent studies have also shown correlations between the dysregulation of microRNA and the development of autoimmune diseases. Autoimmune diseases are a class of disorders that occur when the body develops an immune response to self-antigens. T cells, part of the immune system, change with the environment and can have a significant impact on autoimmunity. T helper type 17 (Th17) cells release cytokines that activate parts of the immune system such as macrophages and neutrophils (Liu et al., 2018). This increases inflammation and immune response throughout the body. However, there are two types of regulatory T (Treg) cells that have the opposite effect. Naturally occurring Treg (nTreg) cells inhibit inflammation and autoimmunity through cell communication, and inducible Treg (iTreg) cells activate cytokines that also have suppressive properties (Liu et al., 2018). In order to maintain homeostasis in the human body, it is important that Th17 cells and Treg cells are balanced. Upregulation of the gene that codes for Th17 causes increased inflammation and an increased risk of developing autoimmune diseases. Similarly, the downregulation of genes that code for Treg cells also causes increased autoimmunity. The relationship between these two types of T cells is crucial for the human body to function properly. MicroRNA also plays a role in the gene regulation of these two cell types, therefore impacting their balance and overall autoimmunity. Upregulation of certain microRNAs inhibits tensin homolog and phosphatases, the result highly activated T cells in immune response. MiR-214 and miR-182 are specifically known for having this effect (Colamatteo et al., 2019). MiR-155 seems to play a role in the suppression and activation of cytokines, and studies in mice have shown evidence that downregulation of miR-146 causes both inflammation autoimmunity to increase, as well as an overall suppression of T cells (Colamatteo et al., 2019). Altogether, an upregulation of miRNAs that control the response of Th17 can lead to chronic inflammation and autoimmunity. Similarly,
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