Effects of environmental stressors on histone modifications and their relevance to carcinogenesis: A systematic review

Dik, Sander; Scheepers, Paul T.J.; Godderis, Lode

doi:10.3109/10408444.2012.684146

Cited by 16 publications

(6 citation statements)

References 36 publications

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“…Major epigenetic mechanisms mainly include DNA methylation, histone modifications, and RNA interference through non-coding RNAs (65). For example, DNA methylation can cause inactivation of genes, and some histone modifications can lead to activation of genes, but these factors are usually dynamic and can be affected by environmental factors (65–67). In addition, non-coding RNAs, such as microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), can also regulate the expressions of targeted genes (68, 69).…”

Section: Introductionmentioning

confidence: 99%

The Emerging Role of Epigenetics in Autoimmune Thyroid Diseases

et al. 2017

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Autoimmune thyroid diseases (AITD) are a group of both B cell- and T cell-mediated organ-specific autoimmune diseases. Graves’ disease and Hashimoto thyroiditis are the two main clinical presentations of AITD. Both genetic and environmental factors have important roles in the development of AITD. Epigenetics have been considered to exert key roles in integrating those genetic and environmental factors, and epigenetic modifications caused by environmental factors may drive genetically susceptibility individuals to develop AITD. Recent studies on the epigenetics of AITD have provided some novel insights into the pathogenesis of AITD. The aim of this review is to provide an overview of recent advances in the epigenetic mechanisms of AITD, such as DNA methylation, histone modifications, and non-coding RNAs. This review highlights the key roles of epigenetics in the pathogenesis of AITD and potential clinical utility. However, the epigenetic roles in AITD are still not fully elucidated, and more researches are needed to provide further deeper insights into the roles of epigenetics in AITD and to uncover new therapeutic targets. Although there are many studies assessing the epigenetic modifications in AITD patients, the clinical utility of epigenetics in AITD remains poorly defined. More studies are needed to identify the underlying epigenetic modifications that can contribute to accurate diagnosis of AITD, adequate choice of treatment approach, and precise prediction of treatment outcomes.

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Section: Introductionmentioning

confidence: 99%

The Emerging Role of Epigenetics in Autoimmune Thyroid Diseases

et al. 2017

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“…The disruption of a normal pattern of covalent histone modifications is an epigenetic event frequently observed upon chemical exposure (Arita et al, 2012;Dik et al, 2012;Sadikovic et al, 2008). In order to determine whether or not furan treatment caused any alterations in histone lysine modifications, the levels of H3K9ac, H3K27ac, H3K56ac, H3K4me1, H3K4me2, H3K4me3, H3K9me3, H3K27me3, H4K20me1, and H4K20me3 were examined using Western immunoblotting in the livers of control rats and rats exposed to furan ( Fig.…”

Section: Effect Of Furan Stop-exposure On Histone Lysine Acetylation mentioning

confidence: 99%

Persistence of Furan-Induced Epigenetic Aberrations in the Livers of F344 Rats

Conti

Kobets

Tryndyak

et al. 2014

Toxicological Sciences

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Furan is a heterocyclic organic compound produced in the chemical manufacturing industry and also found in a broad range of food products, including infant formulas and baby foods. Previous reports have indicated that the adverse biological effects of furan, including its liver tumorigenicity, may be associated with epigenetic abnormalities. In the present study, we investigated the persistence of epigenetic alterations in rat liver. Male F344 rats were treated by gavage 5 days per week with 8 mg furan/kg body weight (bw)/day for 90 days. After the last treatment, rats were divided randomly into 4 groups; 1 group of rats was sacrificed 24 h after the last treatment, whereas other groups were maintained without further furan treatment for an additional 90, 180, or 360 days. Treatment with furan for 90 days resulted in alterations in histone lysine methylation and acetylation, induction of base-excision DNA repair genes, suggesting oxidative damage to DNA, and changes in the gene expression in the livers. A majority of these furan-induced molecular changes was transient and disappeared after the cessation of furan treatment. In contrast, histone H3 lysine 9 and H3 lysine 56 showed a sustained and time-depended decrease in acetylation, which was associated with formation of heterochromatin and altered gene expression. These results indicate that furan-induced adverse effects may be mechanistically related to sustained changes in histone lysine acetylation that compromise the ability of cells to maintain and control properly the expression of genetic information.

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“…The risk factors for lung cancer are usually identified by comparing the studied feature between healthy subjects and lung cancer patients. This approach has determined a series of risk factors, both genetic and epigenetic (1)(2)(3)(4)(5)(6)(7). Since the association between lung cancer and chronic obstructive pulmonary disease (COPD) has been reported in numerous studies (8)(9)(10)(11)(12), the risk factors that influence the morbidity of lung cancer in subjects with COPD constitute a separate problem.…”

Section: Introductionmentioning

confidence: 99%

Carcinogenesis‑related changes in iron metabolism in chronic obstructive pulmonary disease subjects with lung cancer

et al. 2018

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Chronic obstructive pulmonary disease (COPD) is often accompanied by lung cancer. In our previous work, it was observed that matrix metalloproteinase-3 and haptoglobin (HP) polymorphisms were potential markers of enhanced susceptibility to lung cancer development among male COPD subjects. Here, results are reported on blood serum levels of several proteins involved in iron metabolism, inflammation and the oxidative stress response compared between the same groups of subjects. The blood serum levels of tumor necrosis factor α (TNFα), transferrin, hepcidin, ferritin, soluble transferrin receptor and 8-oxo-2'-deoxyguanosine were compared, as well as total iron-binding capacity (TIBC) and ceruloplasmin ferroxidase activity in two groups of subjects: Male COPD patients (54 subjects) and male COPD patients diagnosed with lung cancer (53 subjects). Statistically significant differences were identified between the two groups in transferrin and TNFα levels, as well as in TIBC; all three parameters were lower in the group consisting of COPD patients diagnosed with lung cancer (P<0.01). It was also revealed that HP genotype 1/2 was concomitant with low transferrin blood level in subjects with COPD; this apparent dependence was absent in the COPD + cancer subjects. The results indicate a role of iron metabolism in the susceptibility to lung cancer in COPD-affected subjects. They also emphasize the importance of individual capacity for an effective response to oxidative stress during the pathogenic process as HP is a plasma protein that binds free hemoglobin and its polymorphism results in proteins with altered hemoglobin-binding capacity and different antioxidant and iron-recycling functions.

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Effects of environmental stressors on histone modifications and their relevance to carcinogenesis: A systematic review

Cited by 16 publications

References 36 publications

The Emerging Role of Epigenetics in Autoimmune Thyroid Diseases

The Emerging Role of Epigenetics in Autoimmune Thyroid Diseases

Persistence of Furan-Induced Epigenetic Aberrations in the Livers of F344 Rats

Carcinogenesis‑related changes in iron metabolism in chronic obstructive pulmonary disease subjects with lung cancer

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