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Conjugated Poly/Oligo-Electrolytes for Cancer Diagnosis and Therapy
Published in John R. Reynolds, Barry C. Thompson, Terje A. Skotheim, Conjugated Polymers, 2019
Lingyun Zhou, Guillermo C. Bazan, Shu Wang
DNA methylation is an epigenetic regulation method of gene expression. Hypermethylation of the CpG islands which contain a high frequency of 5'-C-phosphate-G-3' (CpG) sites in promoter regions of tumor suppressor genes can downregulate or inhibit its expression, leading to abnormal cell proliferation. With the aid of the interaction between CCP and DNA, together with FRET from CCP to fluorescently labeled dNTP, like the method used in the detection of SNP, CCP can also be applied in the detection of DNA methylation. The procedure uses bisulfite treatment to replace cytosine by uracil. In the wild type DNA, i.e. without methylation, the cytosine of the CpG site was modified into uracil upon bisulfite treatment, and the uracil was substituted by thymine after PCR amplification. For methylated CpG sites, the cytosine remains unchanged. Fluorescein labeled dGTP and a specific primer, whose 3′-terminal base is C, complementary to the target sequence from methylated DNA region was used in the performance of SBE. The dGTP-Fl was incorporated into the probe by extension reaction for methylation DNA but not the wild type. Upon addition of the cationic conjugated polyelectrolyte PFP1, efficient FRET from PFP1 to fluorescein takes place on methylation groups. In contrast, FRET was sharply weakened for the wild type case. Utilizing another primer, whose 3′-terminal base is T, the FRET would change over, which means, FRET will occur on wild type group rather than methylation groups (Figure 24.12).88
DNA methylation modifications induced by hexavalent chromium
Published in Journal of Environmental Science and Health, Part C, 2019
Xinnian Guo, Lingfang Feng, Bernardo Lemos, Jianlin Lou
DNA methylation is catalyzed by DNA methyl transferases (DNMTs), which is the process of covalent addition of a methyl group to the carbon-5 position of cytosine (C) to form the fifth base, 5-methylcytosine (5mC), in cytosine–guanine (CpG) dinucleotide.21 The regions of the genome that are rich of CpG sequence are called CpG islands, the length of which has to exceed 200 bp, the CG content in which has to be more than 50%.22 CpGs are most often located in the promoter region of the gene 5 prime and the first exon. CpG sites outside the CpG islands are usually methylated, while those inside the CpG islands are non-methylated. Abnormal methylation of CpG sites can cause diseases, such as genetic diseases and cancers.23–25 The evidence from previous studies showed that DNA hypermethylation of specific gene and genome hypomethylation were both related to carcinogenesis.26–32
Epigenotoxicity: a danger to the future life
Published in Journal of Environmental Science and Health, Part A, 2023
Farzaneh Kefayati, Atoosa Karimi Babaahmadi, Taraneh Mousavi, Mahshid Hodjat, Mohammad Abdollahi
One of the most widely studied genetic modifications is DNA methylation. CpG islands are genomic regions that are enriched in CpG sites and are hypomethylated.[9] As a result, hypermethylation alters the regulatory parts of genes present in these islets and causes changes in gene expression.[10]