2021
DOI: 10.1016/j.scitotenv.2020.143175
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Epigenetic alterations induced by aflatoxin B1: An in vitro and in vivo approach with emphasis on enhancer of zeste homologue-2/p21 axis

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Cited by 12 publications
(5 citation statements)
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“…Expression of lncRNAVNN3 was upregulated within exposed workers and treated human lymphocytes; a positive correlation was noted between this lncRNA and serum autophagy-and apoptosis-associated proteins [104]. H2AK119Ub [112]; this cascade of epigenetic events resulted in the deregulation of cell cycle regulatory molecules. A secondary study of aflatoxin B1 treatment within human epithelial cells showed the enhancement of DNA methyltransferases (DNMT1, DNMT3A, and 3B), histone modifiers (HDAC 1, 2, 4, and 6), and histone marks (H2K27me3 and H2AK119Ub) [113].…”
Section: Non-coding Rnasmentioning
confidence: 95%
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“…Expression of lncRNAVNN3 was upregulated within exposed workers and treated human lymphocytes; a positive correlation was noted between this lncRNA and serum autophagy-and apoptosis-associated proteins [104]. H2AK119Ub [112]; this cascade of epigenetic events resulted in the deregulation of cell cycle regulatory molecules. A secondary study of aflatoxin B1 treatment within human epithelial cells showed the enhancement of DNA methyltransferases (DNMT1, DNMT3A, and 3B), histone modifiers (HDAC 1, 2, 4, and 6), and histone marks (H2K27me3 and H2AK119Ub) [113].…”
Section: Non-coding Rnasmentioning
confidence: 95%
“…Since 2016, the effects of benzene on histone marks have only been investigated within human cell lines. As summarized above, crosstalk was identified between histone modifications and genome methylation following AFB1 exposure, specifically the association between repressive histone marks (H3K27me3 and H2AK119Ub) and DNMTs [112,113]. Chromatin immunoprecipitation analysis showed increased enrichment of H3K27me3 following AFB1 exposure upregulated DNMT3a, causing promoter demethylation (Cyclin D1) and hypermethylation (p21).…”
Section: Histone Modificationsmentioning
confidence: 97%
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“…Additionally, AFB1 might greatly inhibit the immune response, raising the risk of cirrhosis and HCC in those with chronic hepatitis B virus infection [ 43 , 44 ]. Excess reactive oxygen species (ROS) production, DNA damage, oxidative stress, lipid peroxidation, apoptosis, mitochondrial dysfunction, autophagy, necrosis, and inflammatory response were all implicated in the pathways of AFB1-induced cytotoxicity or cell death [ 45 , 46 , 47 , 48 , 49 , 50 ]. A number of signaling pathways, such as those involving p53, p21, phosphatidylinositide 3-kinase (PI3K), protein kinase B (PKB, also known as Akt), mammalian target of rapamycin (mTOR), NF-E2-related factor 2 (Nrf2), antioxidant responsive element (ARE), nuclear factor kappa-B (NF-κB), Toll-like receptor 4 (TLR4), TLR2, NOD-like receptor thermal protein domain associated protein 3 (NLRP3)/Caspase-1, mitogen-activated protein kinases (MAPKs), and Wnt/β-catenin pathways, were exemplified to participate in AFB1-induced toxic effects in in vitro and in vivo models [ 45 , 46 , 47 , 48 , 49 , 50 ].…”
Section: An Overview Of Afb1-induced Toxic Effects and Molecular Mech...mentioning
confidence: 99%
“…1,2 Due to their high carcinogenicity, the International Agency for Research on Cancer classifies them as the first category of carcinogens. 3,4 Hence, many countries have established different activity levels for AFs (e.g., 20 ppb of total AFs for food in the U.S.; 5 to 20 ppb of AFB 1 for grains and beans in China). 5 It is essential to develop simple, fast, and cost-effective methods to detect AFs.…”
Section: Introductionmentioning
confidence: 99%