ABSTRACT
Background: Melanoma has been known as an aggressive type of skin cancer in recent years. Reports have distributed the spread rate of melanoma among white skin populations. Also, many studies have mentioned several causes of melanoma. Ultraviolet radiation was represented to be the most important reason for occurrence of melanoma. However, recent studies have found that a combination of factors, such as environmental and genetic factors, can contribute to occurrence of various cancers, specifically melanoma. Methods: Different studies have been conducted on the efficacy of genetic disorders in melanoma. These surveys marked the key role of specific biomarkers in molecular and cellular processes, and investigations have found the expression of several genes in these processes. In addition, aberrant expression of these genes due to mutation and methylation can affect the whole process. Results: The expression process of these genes is regulated by microRNAs. These new biomolecules have been considered as negative regulators because of managing molecular and cellular processes. MicroRNAs are small conserved regulators attached to their targets leading to rearrangement of gene expression. Adherence of these noncoding RNAs can cause mRNA degradation or inhibit its translation. Conclusion: Recently, the application of specific genes in melanoma has been studied. In this review, the way melanoma is regulated because of these biomarkers and their demand through cell cycle in diagnosis, prognosis, and therapeutic periods was considered. Keywords: Melanoma, Biomarkers, Cell cycle, Biomolecules.
ABSTRACT
BACKGROUND: New insights on cellular and molecular aspects of both oligodendrocyte (OL) differentiation and myelin synthesis pathways are potential avenues for developing a cell-based therapy for demyelinating disorders comprising multiple sclerosis. MicroRNAs (miRNA) have broad implications in all aspects of cell biology including OL differentiation. MiR-184 has been identified as one of the most highly enriched miRNAs in oligodendrocyte progenitor cells (OPCs). However, the exact molecular mechanism of miR-184 in OL differentiation is yet to be elucidated. METHODS AND RESULTS: Based on immunochemistry assays, qRT-PCR, and western blotting findings, we hypothesized that overexpression of miR-184 in either neural progenitor cells (NPCs) or embryonic mouse cortex stimulated the differentiation of OL lineage efficiently through regulating crucial developmental genes. Luciferase assays demonstrated that miR-184 directly represses positive regulators of neural and astrocyte differentiation, i.e., SOX1 and BCL2L1, respectively, including the negative regulator of myelination, LINGO1. Moreover, blocking the function of miR-184 reduced the number of committed cells to an OL lineage. CONCLUSIONS: Our data highlighted that miR-184 could promote OL differentiation even in the absence of exogenous growth factors and propose a novel strategy to improve the efficacy of OL differentiation, with potential applications in cell therapy for neurodegenerative diseases.