Epigenetic alteration of mismatch repair genes in the population chronically exposed to arsenic in West Bengal, India

Bhattacharjee, Pritha; Sanyal, Tamalika; Bhattacharjee, Sandip

doi:10.1016/j.envres.2018.01.002

Cited by 38 publications

(17 citation statements)

References 70 publications

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“…It is believed that NNK can affect the level of proteins related to DNA repair mechanisms by inducing the formation of pyridyloxobutyl and methyl adducts [77]. Specifically, NNK-induced DNA methylation, like promoter hyper-methylation of MLH1 and MSH2 [78,79], can significantly affect the ability of cells to repair genetic damage [80]. Therefore, the observed NNK-induced alterations of the MMR gene expression presented here cannot rule out their epigenetic regulation through the NNK-induced DNA methylation.…”

Section: Discussionmentioning

confidence: 72%

The Effect of NNK, A Tobacco Smoke Carcinogen, on the miRNA and Mismatch DNA Repair Expression Profiles in Lung and Head and Neck Squamous Cancer Cells

Doukas

Vageli²,

Lazopoulos

et al. 2020

Cells

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Tobacco smoking is a common risk factor for lung cancer and head and neck cancer. Molecular changes such as deregulation of miRNA expression have been linked to tobacco smoking in both types of cancer. Dysfunction of the Mismatch DNA repair (MMR) mechanism has also been associated with a poor prognosis of these cancers, while a cross-talk between specific miRNAs and MMR genes has been previously proposed. We hypothesized that exposure of lung and head and neck squamous cancer cells (NCI and FaDu, respectively) to tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is capable of altering the expression of MSH2 and MLH1, key MMR components, by promoting specific miRNA deregulation. We found that either a low (1 µM) or high (2 µM) dose of NNK induced significant upregulation of "oncomirs" miR-21 and miR-155 and downregulation of "tumor suppressor" miR-422a, as well as the reduction of MMR protein and mRNA expression, in NCI and FaDu, compared to controls. Inhibition of miR-21 restored the NNK-induced reduced MSH2 phenotype in both NCI and FaDu, indicating that miR-21 might contribute to MSH2 regulation. Finally, NNK exposure increased NCI and FaDu survival, promoting cancer cell progression. We provide novel findings that deregulated miR-21, miR-155, and miR-422a and MMR gene expression patterns may be valuable biomarkers for lung and head and neck squamous cell cancer progression in smokers.Cells 2020, 9, 1031 2 of 22 and neck squamous cell carcinoma (HNSCC), represents one of the most aggressive malignancies with a high rate of mortality. [8,9]. Tobacco smoking has been one of the most well-established risk factors for both lung and head and neck cancers [1][2][3][4][5][6][7][8]. It is known that tobacco smoke contains a mixture of thousands of compounds, including a large number of known carcinogens [2]. It is believed that exposure of cells to tobacco smoke carcinogens can lead to DNA damage, which may cause chromosomal instability and increased cell proliferation [10][11][12][13]. In particular, tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), which is one of the chemicals in tobacco smoke, has been linked to lung and head and neck cancer [14], and has also been shown to upregulate oncogenic pathways [15][16][17].The development and progression of lung and head and neck malignancies appear to be a complex process. Although multiple diagnostic and prognostic markers have been identified for both lung and head and neck cancers [18,19], the precise molecular mechanisms involved in the development and progression of these malignancies remain unclear.We understand that a functional DNA repair mechanism that includes the recognition and repair of mismatch DNA errors during DNA replication is essential in eliminating the harmful effect of several environmental risk factors, such as NNK, on the exposed cells [20][21][22][23]. A number of studies have shown that reduced expression of mismatch DNA repair (MMR) genes increases the incidence of microsatellite ...

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Section: Discussionmentioning

confidence: 72%

The Effect of NNK, A Tobacco Smoke Carcinogen, on the miRNA and Mismatch DNA Repair Expression Profiles in Lung and Head and Neck Squamous Cancer Cells

Doukas

Vageli²,

Lazopoulos

et al. 2020

Cells

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“…However, none of the studies particularly differentiate the degree of altered PTHM between arsenic-exposed skin lesion phenotypes compared to those with no skin lesion. Recently, our group has reported about two different PTHMs among chronic arsenic-exposed population from India considering the skin lesion status ( 38 , 116 ). We identified significant upregulation of H3K79me1 in individuals with arsenic-induced skin lesion, and H3K79me1 was found to be regulated by the upstream methyltransferase DOT1L.…”

Section: Understanding the Present State Of Researchmentioning

confidence: 99%

Recent Advances in Arsenic Research: Significance of Differential Susceptibility and Sustainable Strategies for Mitigation

Sanyal

Bhattacharjee

Paul

2020

Front. Public Health

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Arsenic contamination in drinking water and associated adverse outcomes are one of the major health issues in more than 50 countries worldwide. The scenario is getting even more detrimental with increasing number of affected people and newer sites reported from all over the world. Apart from drinking water, the presence of arsenic has been found in various other dietary sources. Chronic arsenic toxicity affects multiple physiological systems and may cause malignancies leading to death. Exposed individuals, residing in the same area, developed differential dermatological lesion phenotypes and varied susceptibility toward various other arsenic-induced disease risk, even after consuming equivalent amount of arsenic from the similar source, over the same duration of time. Researches so far indicate that differential susceptibility plays an important role in arsenic-induced disease manifestation. In this comprehensive review, we have identified major population-based studies of the last 20 years, indicating possible causes of differential susceptibility emphasizing arsenic methylation capacity, variation in host genome (single nucleotide polymorphism), and individual epigenetic pattern (DNA methylation, histone modification, and miRNA expression). Holistic multidisciplinary strategies need to be implemented with few sustainable yet cost-effective solutions like alternative water source, treatment of arsenic-contaminated water, new adaptations in irrigation system, simple modifications in cooking strategy, and dietary supplementations to combat this menace. Our review focuses on the present perspectives of arsenic research with special emphasis on the probable causes of differential susceptibility toward chronic arsenic toxicity and sustainable remediation strategies.

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“…As inhibits DDR at several levels including DNA repair and cell cycle, and is involved in carcinogenesis. At levels of DNA repair response, As interferes with NER, BER, and MMR . Arsenite suppresses the expression of vital genes in a DNA repair system .…”

Section: Mechanisms Of Ddr/repair In Cancer: Trace Elements Implicationmentioning

confidence: 99%

“…Moreover, As and its metabolite can inhibit MLH1, MSH2, MSH4, and MSH6 . It was revealed in one study that As‐exposed individuals, as opposed to those unexposed to it, experience promoter hypermethylation of MLH1 and MSH2 with consequent downregulation in their gene expression of MLH1 and MSH2 . Moreover, As may inhibit MMR via promoting EGFR expression and PCNA phosphorylation .…”

Section: Mechanisms Of Ddr/repair In Cancer: Trace Elements Implicationmentioning

confidence: 99%

The crosstalk between trace elements with DNA damage response, repair, and oxidative stress in cancer

Tehrani

Hosseini

Yousefi

et al. 2018

J of Cellular Biochemistry

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DNA damage response (DDR) is a regulatory system responsible for maintaining genome integrity and stability, which can sense and transduce DNA damage signals. The severity of damage appears to determine DDRs, which can include damage repair, cell‐cycle arrest, and apoptosis. Furthermore, defective components in DNA damage and repair machinery are an underlying cause for the development and progression of various types of cancers. Increasing evidence indicates that there is an association between trace elements and DDR/repair mechanisms. In fact, trace elements seem to affect mediators of DDR. Besides, it has been revealed that oxidative stress (OS) and trace elements are associated with cancer development. In this review, we discuss the role of some critical trace elements in the risk of cancer. In addition, we provide a brief introduction on DDR and OS in cancer. Finally, we will further review the interactions between some important trace elements including selenium, zinc, chromium, cadmium, and arsenic, and DDR, and OS in cancer.

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Epigenetic alteration of mismatch repair genes in the population chronically exposed to arsenic in West Bengal, India

Cited by 38 publications

References 70 publications

The Effect of NNK, A Tobacco Smoke Carcinogen, on the miRNA and Mismatch DNA Repair Expression Profiles in Lung and Head and Neck Squamous Cancer Cells

The Effect of NNK, A Tobacco Smoke Carcinogen, on the miRNA and Mismatch DNA Repair Expression Profiles in Lung and Head and Neck Squamous Cancer Cells

Recent Advances in Arsenic Research: Significance of Differential Susceptibility and Sustainable Strategies for Mitigation

The crosstalk between trace elements with DNA damage response, repair, and oxidative stress in cancer

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