Résumé
Prostate cancer is one of the leading cause of male cancer-related death worldwide, and the treatment of high-risk prostate cancer and castration resistant prostate cancer remains a significant challenge. Epigenetic modification has been paid more attention in the field of tumor, as a common RNA modification in eukaryotic cells, N6-methyladenosine (m6A) methylation is a dynamic and reversible process regulated by m6A methyltransferase, demethylase and recognition protein, which can regulate the physiological process and tumor progression by regulating gene expression. m6A modification plays an important role in the occurrence and development of prostate cancer and is expected to become a new target in diagnosis, treatment and prognosis. This article reviews the m6A modification and its expression, function and mechanism in prostate cancer, as well as new ideas for clinical application.
Résumé
N6-methyladenine(m6 A),a major RNA methylation modification,affects the development and progression of hu-man cancer through a variety of mechanisms. The m6 A modification also affects multiple aspects of RNA metabolism,ranging from RNA processing,nuclear export,RNA translation to decay. In this review,the basic concepts of m6 A methylation,regulation of m6 A methyltransferase complex and m6 A demethylases in several cancers and some m6 A performed the biological function of the modifica-tion as m6 A-binding proteins are introduced. In addition,the dual role of m6 A methylation and its potential in clinical application are summarized in this review.
Résumé
Objective@#To investigate whether N6-methyladenine DNA(6-mA DNA) modification is related to the occurrence of infantile hemangiomas (IH) at the epigenetic level.@*Methods@#The genomic 6-mA DNA data were obtained by MeDIP and high-throughput sequencing. The 6-mA DNA methylation levels in 3 proliferative hemangioma specimens and adjacent skin tissues were compared by u-test. The functional differences of 6-mA modified genes were analyzed by GO analysis.@*Results@#The level of 6-mA DNA modification in IH tissue was higher. The coverage of 6-mA Peaks in the genome was 0.037% in the tumor tissue, and the coverage of 6-mA Peaks in the surrounding skin tissue was 0.013% in the genome. The difference between the two groups was statistically significant (u=5999.87, P=0.00). The gene functions of differentially 6-mA modified genes in tumors were enriched in mesoderm development, stem cell differentiation, mesenchymal development, and cell cycle. These gene functions were closely related to the pathogenesis of IH.@*Conclusion@#Abnormal 6-mA DNA modification may be one of the pathogenesis of infantile hemangioma.