RESUMEN
Myeloid-derived suppressor cells (MDSCs) are a heterogeneous cell population with potent immunosuppressive functions. They play major roles in cancer and many of the pathologic conditions associated with inflammation. Long non-coding RNAs (lncRNAs) are untranslated functional RNA molecules. The lncRNAs are involved in the control of a wide variety of cellular processes and are dysregulated in different diseases. They can participate in the modulation of immune function and activity of inflammatory cells, including MDSCs. This mini review focuses on the emerging role of lncRNAs in MDSC activity. We summarize how lncRNAs modulate the generation, recruitment, and immunosuppressive functions of MDSCs and the underlying mechanisms.
Asunto(s)
Inflamación/inmunología , Células Supresoras de Origen Mieloide/inmunología , Neoplasias/inmunología , ARN Largo no Codificante/fisiología , Animales , Proteína beta Potenciadora de Unión a CCAAT/fisiología , Linaje de la Célula , Epigénesis Genética , Predicción , Regulación Neoplásica de la Expresión Génica/inmunología , Humanos , Inmunoterapia , Ratones , Células Supresoras de Origen Mieloide/clasificación , Neoplasias/genética , Neoplasias/terapia , Óxido Nítrico/metabolismo , Seudogenes , ARN Largo no Codificante/genética , ARN Largo no Codificante/inmunología , ARN Neoplásico/inmunología , ARN Neoplásico/fisiología , Especies Reactivas de Oxígeno/metabolismo , Escape del Tumor , Microambiente TumoralRESUMEN
OBJECTIVE: Epigenetic mechanisms, such as DNA methylation, regulate important biological processes as gene expression and it was suggested that these phenomena play important roles in the carcinogenesis and tumor biology. The aim of this review is to provide the current state of knowledge about epigenetic alterations, focusing mainly on DNA methylation, reported in odontogenic tumors. DESIGN: Literatures were searched based in the combination of the following keywords: odontogenic tumors, epigenetics, DNA methylation, histone modifications, non-coding RNA, microRNA, DNA methyltransferases. Electronic databases (Medline/PubMed, Scopus and Web of Science) were screened. RESULTS: The analysis of epigenetic alterations in different tumors has rapidly increased; however, limited information is available about epigenetic mechanisms involved in the formation of odontogenic tumors. DNA methylation is the most studied epigenetic modification in these tumors and the participation of non-coding RNA's in odontogenic tumors has been recently addressed. Differential expression of DNA methyltransferases, altered DNA methylation patterns and aberrant expression of non-coding RNA's were reported in odontogenic tumors. CONCLUSIONS: Current studies suggest epigenetics as an emerging mechanism, possibly implicated in etiopathogenesis of odontogenic tumors. Deeper understanding of the epigenetic abnormalities in these tumors could show potential applications as biomarkers or therapeutic possibilities in the future.
Asunto(s)
Metilación de ADN , Epigénesis Genética , Tumores Odontogénicos/genética , Expresión Génica , HumanosRESUMEN
Chromatin in cervical cancer (CC) undergoes chemical and structural changes that alter the expression pattern of genes. Recently, a potential mechanism, which regulates gene expression at transcriptional levels is the proteolytic clipping of histone H3. However, until now this process in CC has not been reported. Using HeLa cells as a model of CC and human samples from patients with CC, we identify that the H3 cleavage was lower in CC compared with control tissue. Additionally, the histone H3 clipping was performed by serine and aspartyl proteases in HeLa cells. These results suggest that histone H3 clipping operates as part of post-translational modification system in CC.
