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Genetic and Epigenetic Considerations in iPSC Technology
Published in Deepak A. Lamba, Patient-Specific Stem Cells, 2017
Histone deacetylase (HDAC) family includes 11 proteins in mammals (HDAC1-11). The NuRD complex is proposed to promote the deacetylation of H3K27ac by introducing HDACs. The core components of NuRD complex is composed of RbAp48, MBD3, HDAC1/2, Mi-2 (CHD4), p66, and MTA1 (133). Mi-2 contains chromodomain, which is required for ATP-dependent nucleosome remodeling. MTA1 may facilitate binding to DNA, and the role of p66 is still unknown. In ESCs, the knockdown of Mbd3 accelerates self-renewal in the absence of LIF, while Mta1 knockdown enhances differentiation (134). iPSC reprogramming is inhibited by Mbd3 (135) but is facilitated by the co-expression of Mbd3 and Nanog (136). In addition, NuRD-mediated H3K27 deacetylation is promoted by the recruitment of PRC2 (137). Overall, although the gain and the maintenance of H3K27ac are required for self-renewal, reprogramming and differentiation are each regulated by distinct enzymes.
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
Liver cancer can be divided into different types. The main two types of it are hepatocellular carcinoma (HCC) and hepatoblastoma (HBL), which correlates with hepatocyte cells.[161] A cohort study on 74 surgical specimens showed a global DNA methylation and its relation with the PRC2 complex in HCC responsible for cell reprogramming.[162] Another examination on HBL sample tissues reported an elevated HDAC1 expression in HBL; subsequently, CIEBPα protein and SP5 transcription factor gene were overexpressed. These pathways are responsible for HBL onset by the mediation of epigenetic regulation.[161]In vivo and in vitro study using human hepatoma cell line Hep3B demonstrated that overexpression of miR-155 in HCC inhibits H3F3A and the H3K27me1/2/3 modifications, as well as suppression of P21WAF1/CIP1 via increases the CDK2 phosphorylation; thus it has a key role in liver cancer growth and development.[163] Aflatoxin B1 (AFB1) is a mycotoxin that causes gene mutation via DNA interaction and forming AFB1-adducts. Studies claimed that alteration in the DNA methylation pattern of some genes can synergically help this mutation in HCC.[215]