Channels • 2021 • Volume 6 • Number 1 Page 5 miRNAs and oncomiRs contributes to the progression of various cancer types, and current researchers search for ways to correct the expression of certain microRNAs to possibly treat or slow the progression of cancer types. By understanding which miRNAs are differentially expressed in glioblastoma tumors and discovering how to control the expression of certain miRNAs, it may be possible to minimize or even reverse the effects of glioblastoma and lower the fatality rate of this type of brain tumor. When tumor-suppressing microRNAs lose function, malignant tumors can form. As previously discussed, microRNAs are responsible for regulating gene expression, and cancer research primarily focuses on the expression of tumor suppressor proteins and proto-oncogenes. Tumor suppressor microRNAs act by inhibiting the mRNAs that code for oncogenes. In many malignant tumors, tumor suppressor miRNAs have significantly lost their function through mutations, epigenetic silencing, or mistakes in mRNA processing (Mollaei et al., 2019). Some examples of a loss of function of tumor suppressor miRNAs in malignant tumors are miR-449a and miR495. MiR-449a is known to be downregulated in glioblastoma cells and may be contribute to the aggressive growth and multiplication of these cells. MiR495, on the other hand, is known to be downregulated in breast cancer, prostate cancer, and leukemia (Mollaei et al., 2019). Among many others, these downregulated miRNAs play a role in the development and progression of various cancer types. Another type of miRNA that plays a role in the development of cancer types is oncomiRs. OncomiRs are typically upregulated in cancerous tumor cells because of mutation or misregulation of certain pathways such as histone methylation or promoter methylation (Mollaei et al., 2019). Common miRNAs that are upregulated in cancer cells are miR-155 and miR-21. MiR-155 is overexpressed in lung cancer, breast cancer, and multiple forms of lymphoma, while MiR-21 is overexpressed in almost every type of human cancer—including blood and organ cancers (Mollaei et al., 2019). While little is known about the effects of upregulated miRNAs, it is clear they are important to the development of cancer like tumor suppressor miRNAs are. Understanding the expression of miRNAs and their role in cancer development could lead to development of a treatment for some of the most lethal cancers, such as glioblastoma. Theoretically, upregulating the downregulated tumor suppressor miRNAs or downregulating the upregulated miRNAs could recreate a balance between tumor suppressor proteins and oncogenes. Two current theories exist to explain how this information could be used in a viable treatment: miRNA reduction therapy and miRNA restoration therapy. MiRNA reduction, also called inhibition therapy, is based on the concept of inactivating upregulated miRNAs. Several methods are currently being used to try to meet this end, including miRNA sponges, locked-nucleic-acid antisense oligonucleotides, anti-miRNA oligonucleotides, miRNA nanoparticles, antagomirs, and multiple-target anti-miRNA antisense oligodeoxyribonucleotides (Mollaei et al., 2019). The basis behind all these methods is the same: to inhibit the expression of oncomiRs and slow the progression of various cancer types. However, there are some challenges related to this therapy. For example, many oncomiRs have multiple targets and focusing on limiting one miRNA at a time would not have a noticeable effect on cancer in a clinical setting (Mollaei et al., 2019). The concept behind the other method, miRNA restoration therapy, is to upregulate the tumor suppressor miRNAs and allow them to slow the production of oncoproteins within cancerous cells. The goal of this kind of therapy is to have cancerous cells take up microRNA genetic material that
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