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“Omics”
Published in Kirk A. Phillips, Dirk P. Yamamoto, LeeAnn Racz, Total Exposure Health, 2020
The epigenome broadly refers to molecular marks and mechanisms that control the structural organization of the genome and thus exert an influence on gene expression without changing the actual coding sequence (Rivera and Ren 2013). Epigenetic changes can act as an on/off switch to activate/inactivate large genomic areas (an example being X-chromosome inactivation) or as a “rheostat” finely tuning gene expression. The deposition of epigenetic marks (and thus gene expression levels) is a mechanism by which cell and tissue types are determined. Epigenetic control is achieved most commonly by modifications of DNA or histones or through regulatory RNA. Common epigenetic marks include methylation/demethylation at cytosine residues of cytosine-guanosine dinucleotides (CpG) or histone tails (which can also be modified by acetylation/deacetylation). The modifications at histones modulate chromatin structure and accessibility of transcription factors, while cytosine methylation/hydroxymethylation generally leads to gene silencing through recruitment of repressors like methyl-binding protein domain protein and histone deacetylases. CpG dinucleotides are overrepresented in promoters and regulatory regions and some repetitive DNA elements.
Genes and Genomics
Published in Firdos Alam Khan, Biotechnology Fundamentals, 2020
Epigenetics changes may be reflected at various stages throughout a person’s life; for example, several studies have provided evidence that prenatal and early postnatal environmental factors influence human embryos and may cause the development of various chronic diseases and behavioral disorders in adulthood. For example, studies have shown that children born during the period of the famine from 1944 to 1945 in Holland have shown increased rates of coronary heart disease and obesity after maternal exposure to famine during pregnancy. Similarly, adults that were prenatally exposed to famine conditions have also been reported to have a higher frequency of schizophrenia. Cancer was the first human disease to be linked to epigenetics, for example, research performed by Feinberg and Vogelstein in 1983, found that genes of colorectal cancer cells were significantly hypo-methylated compared with normal tissues. It has been reported that DNA hypo-methylation can activate oncogenes and initiate chromosome instability; however, DNA hyper-methylation initiates silencing of tumor suppressor genes. The buildup of genetic and epigenetic faults can convert a normal cell into a metastatic tumor cell. Furthermore, DNA methylation patterns may cause abnormal expression of cancer-associated genes. The modification of global histone patterns is linked with prostate, breast, and pancreatic cancers. Therefore, epigenetic changes or modifications can be used as biomarkers for the diagnosis of early cancer.
Epigenomic alterations in the individuals exposed to arsenic through drinking water in West Bengal, India
Published in Yong-Guan Zhu, Huaming Guo, Prosun Bhattacharya, Jochen Bundschuh, Arslan Ahmad, Ravi Naidu, Environmental Arsenic in a Changing World, 2019
A.K. Giri, D. Chatterjee, N. Banerjee
Arsenic is not mutagenic but carcinogenic and human. There is a strong believe that arsenic follows the epigenetic pathways to induce cancer in humans. DNA methylation is an epigenetic modification of DNA that is tightly regulated in mammalian development and is responsible for maintaining the normal functioning of the adult organism (Schaefer et al., 2007). Micro RNAs(miRNA) are small 19–25 nucleotides long non-coding RNA molecules that functions in controlling gene expression post-transcriptionally by destabilizing the transcribed mRNA or translational repression (Filipowicz et al., 2008). Evidence showed that epigenetic modifications including DNA methylation and altered micro RNA expression patterns contribute to carcinogenesis (Watanabe et al., 2008). So here we have investigated the epigenetic alterations in arsenic exposed population in West Bengal, India.
Animal models and mechanisms of tobacco smoke-induced chronic obstructive pulmonary disease (COPD)
Published in Journal of Toxicology and Environmental Health, Part B, 2023
Priya Upadhyay, Ching-Wen Wu, Alexa Pham, Amir A. Zeki, Christopher M. Royer, Urmila P. Kodavanti, Minoru Takeuchi, Hasan Bayram, Kent E. Pinkerton
In addition to RNA interference, other epigenetic modifications might be mediated by different mechanisms, including DNA methylation and histone modification, which might also play essential roles in COPD development. DNA methylation is a chemical modification that involves addition of a methyl group to cytosine residues in CpG dinucleotides, resulting in formation of 5-methylcytosine. DNA methylation might occur in promoter regions of genes, leading to gene silencing or reduced gene expression. In COPD, alterations in DNA methylation patterns were noted in genes involved in inflammation, oxidative stress, and tissue remodeling, which are critical processes in COPD pathogenesis (Alfahad et al. 2021). Previously Zeng et al. (2020) suggested that cigarette-induced oxidative stress plays a role in mediating pulmonary apoptosis and hypermethylation of the B-cell lymphoma/leukemia-2 (Bcl-2) promoter, an apoptosis regulator, in COPD through DNA methyltransferase enzyme 1 (DNMT1), a key DNA methyltransferase enzyme. Similarly, aberrant DNA methylation was reported to be a widespread occurrence in small airways of COPD patients and was associated with altered expression of genes and pathways related to COPD, such as NF-E2-related factor 2 oxidative response pathway (Vucic et al. 2014).
Multi-platform analysis of methylation-regulated genes in human lung adenocarcinoma
Published in Journal of Toxicology and Environmental Health, Part A, 2019
Jin Wang, Xiao-fan Yu, Nan OUYang, Qiu-lin Luo, Shi-yu Zhao, Xi-fei Guan, Tao Chen, Jian-xiang Li
DNA methylation plays a critical role in vari-ous biological processes during development, and dysregulation results in pathological consequences (Yin et al. 2012). Klutstein et al. (2016) reported that aberrant DNA methylation is considered as a promising biomarker for early carcinogenesis and resistance to therapy. Using high-throughput methods or targeted approaches, global hypo-methylation and promoter-associated hyper-methylation NSCLC were identified in NSCLC (Carvalho et al. 2012; Field et al. 2005; Fukasawa et al. 2006; Knight et al. 2009). However, the association between LUAD aberrant DNA methylation in humans has not been examined comprehensively.
Role of DNA methylation regulation of miR-130b expression in human lung cancer using bioinformatics analysis
Published in Journal of Toxicology and Environmental Health, Part A, 2019
Jin Wang, Xiao-Fan Yu, Nan OUYang, Qiulin Luo, Jian Tong, Tao Chen, Jianxiang Li
The interaction of DNA with smoking constituents is postulated to play an important role in the observed lung carcinoma in animals and humans. Numerous investigators reported that aberrant DNA methylation contributed to the initiation and subsequent development of many types of cancers (Brock et al. 2008; Chen et al. 2012; Hoque 2009). It is noteworthy that DNA methylation regulates gene expression (Gyorffy et al. 2016). In addition, regulation of gene expression also occurs due stimulation of a special class of small, 19–22 nucleotides long, non-coding RNA, called microRNA (miRNAs) (Ha and Kim 2014).