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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
Histone methyltransferase, G9a, is marked as an enzyme responsible for introducing the H3K9 dimethylation, a hallmark of euchromatin silencing [84,93,104,105]. HP1 (heterochromatin protein 1) binds with H3K9me2, which works in the recruitment of transcriptional repressors that prevent the active gene activation [106]. Although G9a-mediated methylation leads to the production of H3K9me2, the complex of G9a/GLP has also been demonstrated to methylate H1 [107,108] and also shows its contribution to the H3K27 methylation [93,109]. Further, G9a proved to have specific marked activity against numerous non-histone-based proteins by means of including itself, too [110]. However, the most well-studied G9a biology aspect is the repression of H3K9me2-based genetic expression. Moreover, from the various biochemical-based studies, it is clearly understood that G9a-based H3K9me2 is correlated with those regions of the genome that expressed at very low levels [87]. Still, the exact mechanisms that work in dynamic methylation pattern regulation mediated by Ehmt was unclear until now.
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
Benzo[a]pyrene osteotoxicity and the regulatory roles of genetic and epigenetic factors: A review
Published in Critical Reviews in Environmental Science and Technology, 2022
Jiezhang Mo, Doris Wai-Ting Au, Jiahua Guo, Christoph Winkler, Richard Yuen-Chong Kong, Frauke Seemann
Growing evidence suggests that histone modifications serve a critical role in regulating bone metabolism and osteoporosis (Letarouilly et al., 2019; Liu et al., 2015). For instance, histone deacetylation inhibits osteogenesis and osteoclastogenesis in vitro in bone cells treated with histone deacetylase inhibitors (Boer et al., 2006; Cho et al., 2005). Additionally, methylation and demethylation may function as epigenetic switches for bone MSC lineage fate determination (Hemming et al., 2014). The enhancer of zeste homolog 2 (EZH2), is a histone methyltransferase that is capable of catalyzing the trimethylation of histone H3 on lysine 27 (H3K27me3) on its target genes, thereby inhibiting osteogenesis (Dudakovic et al., 2015). Conversely, lysine demethylase 6 A (KDM6A) promotes osteogenesis (Chen et al., 2011). The phosphorylation of EZH2 inhibits its methyltransferase activity and promotes osteogenesis (Wei et al., 2011).
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
The main reason for cervical cancer is papillomavirus, but recent studies showed the effects of epigenetic factors on its onset. By studying 37 cervical tumors and three associated normal tissues, downregulation of 3 genes (GABRA2, ZNF257, and SLC5A8) was observed due to the aberrant DNA methylation.[165] Studying the tissue specimens of 24 cervical cancer cases, 24 matched peri-carcinomatous, and 16 normal cervical cases determined that higher expression of Tim-3 and galectin-9 as costimulatory factors increases immune suppression and tumor development. Higher expression of these factors is regulated by EZH2 histone methyltransferase, H3K27me3, and DNMT3A, which are misregulated in cervical cancer.[166]