RESUMO
Neuroblastoma is known as the most prevalent extracranial malignancy in childhood with a neural crest origin. It has been widely accepted that non-coding RNAs (ncRNAs) play important roles in many types of cancer, including glioma and gastrointestinal cancers. They may regulate the cancer gene network. According to recent sequencing and profiling studies, ncRNAs genes are deregulated in human cancers via deletion, amplification, abnormal epigenetic, or transcriptional regulation. Disturbances in the expression of ncRNAs may act either as oncogenes or as anti-tumor suppressor genes, and can lead to the induction of cancer hallmarks. ncRNAs can be secreted from tumor cells inside exosomes, where they can be transferred to other cells to affect their function. However, these topics still need more study to clarify their exact roles, so the present review addresses different roles and functions of ncRNAs in neuroblastoma.
Assuntos
Neuroblastoma , RNA não Traduzido , Humanos , RNA não Traduzido/genética , Regulação da Expressão Gênica , Oncogenes , Neuroblastoma/genéticaRESUMO
Nowadays, there is an increasing concern regarding traumatic brain injury (TBI) worldwide since substantial morbidity is observed after it, and the long-term consequences that are not yet fully recognized. A number of cellular pathways related to the secondary injury in brain have been identified, including free radical production (owing to mitochondrial dysfunction), excitotoxicity (regulated by excitatory neurotransmitters), apoptosis, and neuroinflammatory responses (as a result of activation of the immune system and central nervous system). In this context, non-coding RNAs (ncRNAs) maintain a fundamental contribution to post-transcriptional regulation. It has been shown that mammalian brains express high levels of ncRNAs that are involved in several brain physiological processes. Furthermore, altered levels of ncRNA expression have been found in those with traumatic as well non-traumatic brain injuries. The current review highlights the primary molecular mechanisms participated in TBI that describes the latest and novel results about changes and role of ncRNAs in TBI in both clinical and experimental research.
Assuntos
Lesões Encefálicas Traumáticas , Lesões Encefálicas , MicroRNAs , RNA Longo não Codificante , Animais , Humanos , Lesões Encefálicas/metabolismo , RNA não Traduzido/genética , RNA não Traduzido/metabolismo , Lesões Encefálicas Traumáticas/genética , Lesões Encefálicas Traumáticas/metabolismo , Encéfalo/metabolismo , Regulação da Expressão Gênica , RNA Longo não Codificante/genética , RNA Longo não Codificante/metabolismo , MicroRNAs/genética , Mamíferos/genéticaRESUMO
Synaptic plasticity is the ability of synapses to weaken or strengthen over time, in response to changes in the activity of the neurons. It is orchestrated by a variety of genes, proteins, and external and internal factors, especially epigenetic factors. MicroRNAs (miRNAs) are well-acknowledged epigenetic modulators that regulate the translation and degradation of target genes in the nervous system. Increasing evidence has suggested that a number of miRNAs play important roles in modulating various aspects of synaptic plasticity. The deregulation of miRNAs could be associated with pathological alterations in synaptic plasticity, which could lead to different CNS-related diseases. Herein, we provide an update on the role of miRNAs in governing synaptic plasticity. In addition, we also summarize recent researches on the role of miRNAs in drug addiction, and their targets and mechanism of action. Understanding of the way in which miRNAs contribute to synaptic plasticity provides rational clues in establishing the novel biomarkers and new therapeutic strategies for the diagnosis and treatment of plasticity-related diseases and drug addiction.
