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Role of Histone Methyltransferase in Breast Cancer
Published in Meenu Gupta, Rachna Jain, Arun Solanki, Fadi Al-Turjman, Cancer Prediction for Industrial IoT 4.0: A Machine Learning Perspective, 2021
Surekha Manhas, Zaved Ahmed Khan
Gene expression regulation by means of histone-modifying enzymes marks a dominant mechanism that regulates the differentiation and development of cells. Posttranslationally, modifications of histones could be carried out by methylation, acetylation, phosphorylation, ubiquitination, and sumoylation [75]. In particular, methylation at lysine residues of histone protein is the chief regulator of active gene expression. MLL1-dependent H3K4me3 and EZH2-dependent H3K27me3 EZH2, H3K27me3, are the foremost well-known modifications that are strongly related to recognizable gene expression also with repression [76–80]. Various other specific histone-methylation regions have been recognized to be more critical, including H3K9 histone residue with G9a-dependent H3K9me2 and Suv39h (1–2)-mediated H3K9me3. All these display crucial functional roles in cellular differentiation and functions, too [81–84]. Available data suggest that H3K9me2 has also been found to modify euchromatin. In addition, it also is dynamically able to regulate the gene expression of many differentiating cells.
Genetic and Epigenetic Considerations in iPSC Technology
Published in Deepak A. Lamba, Patient-Specific Stem Cells, 2017
Trimethylation of H3 lysine 9 (H3K9me3) is another repressive histone mark and is distributed in the heterochromatin (74,75,138). The H3K9me3 domain size in ESCs is significantly larger than that in somatic cells and is the most discordant histone modification between ESCs and iPSCs (100). The differential H3K9me3 region is megabase scale and related to non-CG DNA methylation (6). In addition, H3K9me3 silences the expression of retrotransposons, which is associated with pluripotency and stem cell development (139,140). Since the aberrant H3K9me3 in iPSCs is refractory to OSKM (OCT4, SOX2, KLF4, and C-MYC)-mediated chromatin remodeling, additional factors to displace it is critical in producing truly ESC-like iPSCs (141).
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
Through examining type 1 diabetes mellitus (T1DM), the SNP-CpG genes and DNA methylation in CpGs have been identified as genetic material expression or insulin secretion mediators. Gene methylation, such as GPX7, GSTT1, and SNX19, directly regulate vital biological processes like proliferation and apoptosis in pancreatic β cells. Genetic and epigenetic diversity in the genome impacts gene expression, CpGs function, and the potential risk of diabetes. Monomethylation or trimethylation of H3K4me1 and H3K4me3 activates insulin secretion gene promoters, and trimethylation of histones H3K9me3 and H3K27me3 causes chromatins to be compressed in pancreatic cells and the gene to be silenced. DNA methylation is associated with a lack of H3K4 methylation and the presence of H3K9 methylation. C-Rel and p65 proteins, which belong to the NF-κB family, activate the mir-21 gene promoter in pancreatic β cells and increase miR-21. MiR-21 further reduces PDCD4 protein levels and cell death. Therefore, PDCD4 deficiency in pancreatic β cells makes them resistant to dying. In summary, the NF-κB-microRNA-21-PDCD4 complex is one of the essential factors in T1DM and is one of the most critical factors in studying the development of treatment for this disease.[135]
Toxic and carcinogenic effects of hexavalent chromium in mammalian cells in vivo and in vitro: a recent update
Published in Journal of Environmental Science and Health, Part C, 2022
Shehnaz Islam, Sreejata Kamila, Ansuman Chattopadhyay
Epigenetic modifications by Cr (VI) have been demonstrated in in vitro studies with cell lines. Cr (VI) elicited modifications of histone acetylation and downregulation of biotinidase in human bronchial epithelial cells,86 induced DNA methylation and subsequent silencing of the gpt gene in G12 cell lines.88 Cr (VI)-induced hypermethylation of P16 and TP53 were observed in DNA strand breakage in 16HBE human bronchial epithelial cells.72 Cr (VI) induced hypermethylation of CpG sites in DNA repair genes was correlated with genetic damage and downregulated expression of DNA repair genes in Cr (VI)-exposed 16HBE cells.71 An increase in histone methyltransferase ESET that catalyzes H3-K9 methylation in mammalian cells and the global H3K9me3 and H3K27me3 epigenetic alterations have been observed during exposure to Cr (VI).121