Seyedeh Elham Norollahi, Sogand Vahidi, Shima Shams, Arman Keymoradzdeh, Armin Soleymanpour, Nazanin Solymanmanesh, Ebrahim Mirzajani, Vida Baloui Jamkhaneh, Ali Akbar Samadani
{"title":"癌症DNA甲基化改变的分析和治疗概况;染色质排列的变化和组蛋白表面的变化综述。","authors":"Seyedeh Elham Norollahi, Sogand Vahidi, Shima Shams, Arman Keymoradzdeh, Armin Soleymanpour, Nazanin Solymanmanesh, Ebrahim Mirzajani, Vida Baloui Jamkhaneh, Ali Akbar Samadani","doi":"10.1515/hmbci-2022-0043","DOIUrl":null,"url":null,"abstract":"<p><p>DNA methylation is the most important epigenetic element that activates the inhibition of gene transcription and is included in the pathogenesis of all types of malignancies. Remarkably, the effectors of DNA methylation are DNMTs (DNA methyltransferases) that catalyze <i>de novo</i> or keep methylation of hemimethylated DNA after the DNA replication process. DNA methylation structures in cancer are altered, with three procedures by which DNA methylation helps cancer development which are including direct mutagenesis, hypomethylation of the cancer genome, and also focal hypermethylation of the promoters of TSGs (tumor suppressor genes). Conspicuously, DNA methylation, nucleosome remodeling, RNA-mediated targeting, and histone modification balance modulate many biological activities that are essential and indispensable to the genesis of cancer and also can impact many epigenetic changes including DNA methylation and histone modifications as well as adjusting of non-coding miRNAs expression in prevention and treatment of many cancers. Epigenetics points to heritable modifications in gene expression that do not comprise alterations in the DNA sequence. The nucleosome is the basic unit of chromatin, consisting of 147 base pairs (bp) of DNA bound around a histone octamer comprised of one H3/H4 tetramer and two H2A/H2B dimers. DNA methylation is preferentially distributed over nucleosome regions and is less increased over flanking nucleosome-depleted DNA, implying a connection between nucleosome positioning and DNA methylation. In carcinogenesis, aberrations in the epigenome may also include in the progression of drug resistance. In this report, we report the rudimentary notes behind these epigenetic signaling pathways and emphasize the proofs recommending that their misregulation can conclude in cancer. These findings in conjunction with the promising preclinical and clinical consequences observed with epigenetic drugs against chromatin regulators, confirm the important role of epigenetics in cancer therapy.</p>","PeriodicalId":13224,"journal":{"name":"Hormone Molecular Biology and Clinical Investigation","volume":null,"pages":null},"PeriodicalIF":1.1000,"publicationDate":"2023-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Analytical and therapeutic profiles of DNA methylation alterations in cancer; an overview of changes in chromatin arrangement and alterations in histone surfaces.\",\"authors\":\"Seyedeh Elham Norollahi, Sogand Vahidi, Shima Shams, Arman Keymoradzdeh, Armin Soleymanpour, Nazanin Solymanmanesh, Ebrahim Mirzajani, Vida Baloui Jamkhaneh, Ali Akbar Samadani\",\"doi\":\"10.1515/hmbci-2022-0043\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>DNA methylation is the most important epigenetic element that activates the inhibition of gene transcription and is included in the pathogenesis of all types of malignancies. Remarkably, the effectors of DNA methylation are DNMTs (DNA methyltransferases) that catalyze <i>de novo</i> or keep methylation of hemimethylated DNA after the DNA replication process. DNA methylation structures in cancer are altered, with three procedures by which DNA methylation helps cancer development which are including direct mutagenesis, hypomethylation of the cancer genome, and also focal hypermethylation of the promoters of TSGs (tumor suppressor genes). Conspicuously, DNA methylation, nucleosome remodeling, RNA-mediated targeting, and histone modification balance modulate many biological activities that are essential and indispensable to the genesis of cancer and also can impact many epigenetic changes including DNA methylation and histone modifications as well as adjusting of non-coding miRNAs expression in prevention and treatment of many cancers. Epigenetics points to heritable modifications in gene expression that do not comprise alterations in the DNA sequence. 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Analytical and therapeutic profiles of DNA methylation alterations in cancer; an overview of changes in chromatin arrangement and alterations in histone surfaces.
DNA methylation is the most important epigenetic element that activates the inhibition of gene transcription and is included in the pathogenesis of all types of malignancies. Remarkably, the effectors of DNA methylation are DNMTs (DNA methyltransferases) that catalyze de novo or keep methylation of hemimethylated DNA after the DNA replication process. DNA methylation structures in cancer are altered, with three procedures by which DNA methylation helps cancer development which are including direct mutagenesis, hypomethylation of the cancer genome, and also focal hypermethylation of the promoters of TSGs (tumor suppressor genes). Conspicuously, DNA methylation, nucleosome remodeling, RNA-mediated targeting, and histone modification balance modulate many biological activities that are essential and indispensable to the genesis of cancer and also can impact many epigenetic changes including DNA methylation and histone modifications as well as adjusting of non-coding miRNAs expression in prevention and treatment of many cancers. Epigenetics points to heritable modifications in gene expression that do not comprise alterations in the DNA sequence. The nucleosome is the basic unit of chromatin, consisting of 147 base pairs (bp) of DNA bound around a histone octamer comprised of one H3/H4 tetramer and two H2A/H2B dimers. DNA methylation is preferentially distributed over nucleosome regions and is less increased over flanking nucleosome-depleted DNA, implying a connection between nucleosome positioning and DNA methylation. In carcinogenesis, aberrations in the epigenome may also include in the progression of drug resistance. In this report, we report the rudimentary notes behind these epigenetic signaling pathways and emphasize the proofs recommending that their misregulation can conclude in cancer. These findings in conjunction with the promising preclinical and clinical consequences observed with epigenetic drugs against chromatin regulators, confirm the important role of epigenetics in cancer therapy.
期刊介绍:
Hormone Molecular Biology and Clinical Investigation (HMBCI) is dedicated to the provision of basic data on molecular aspects of hormones in physiology and pathophysiology. The journal covers the treatment of major diseases, such as endocrine cancers (breast, prostate, endometrium, ovary), renal and lymphoid carcinoma, hypertension, cardiovascular systems, osteoporosis, hormone deficiency in menopause and andropause, obesity, diabetes, brain and related diseases, metabolic syndrome, sexual dysfunction, fetal and pregnancy diseases, as well as the treatment of dysfunctions and deficiencies. HMBCI covers new data on the different steps and factors involved in the mechanism of hormone action. It will equally examine the relation of hormones with the immune system and its environment, as well as new developments in hormone measurements. HMBCI is a blind peer reviewed journal and publishes in English: Original articles, Reviews, Mini Reviews, Short Communications, Case Reports, Letters to the Editor and Opinion papers. Ahead-of-print publishing ensures faster processing of fully proof-read, DOI-citable articles.