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Article ; Online: Epigenetics in metal carcinogenesis: nickel, arsenic, chromium and cadmium.

Arita, Adriana / Costa, Max

Metallomics : integrated biometal science

2010 Volume 1, Issue 3, Page(s) 222–228

Abstract: Although carcinogenic metals have been known to disrupt a wide range of cellular processes the precise mechanism by which these exert their carcinogenic effects is not known. Over the last decade or two, studies in the field of metal carcinogenesis ... ...

Abstract	Although carcinogenic metals have been known to disrupt a wide range of cellular processes the precise mechanism by which these exert their carcinogenic effects is not known. Over the last decade or two, studies in the field of metal carcinogenesis suggest that epigenetic mechanisms may play a role in metal-induced carcinogenesis. In this review we summarize the evidence demonstrating that exposure to carcinogenic metals such as nickel, arsenic, chromium, and cadmium can perturb DNA methylation levels as well as global and gene specific histone tail posttranslational modification marks. We also wish to emphasize the importance in understanding that gene expression can be regulated by both genetic and epigenetic mechanisms and both these must be considered when studying the mechanism underlying the toxicity and cell-transforming ability of carcinogenic metals and other toxicants, and aberrant changes in gene expression that occur during disease states such as cancer.
MeSH term(s)	Animals ; Arsenic/toxicity ; Arsenic Poisoning/genetics ; Cell Transformation, Neoplastic/drug effects ; Cell Transformation, Neoplastic/genetics ; DNA Methylation ; Epigenomics ; Gene Expression Regulation, Neoplastic/drug effects ; Heavy Metal Poisoning ; Humans ; Metals, Heavy/toxicity
Chemical Substances	Metals, Heavy ; Arsenic (N712M78A8G)
Language	English
Publishing date	2010-04-30
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2474317-3
ISSN	1756-591X ; 1756-5901
ISSN (online)	1756-591X
ISSN	1756-5901
DOI	10.1039/b903049b
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Article ; Online: Carcinogenic metals and the epigenome: understanding the effect of nickel, arsenic, and chromium.

Chervona, Yana / Arita, Adriana / Costa, Max

Metallomics : integrated biometal science

2012 Volume 4, Issue 7, Page(s) 619–627

Abstract: Carcinogenic metals, such as nickel, arsenic, and chromium, are widespread environmental and occupational pollutants. Chronic exposure to these metals has been connected with increased risks of numerous cancers and as well as non-carcinogenic health ... ...

Abstract	Carcinogenic metals, such as nickel, arsenic, and chromium, are widespread environmental and occupational pollutants. Chronic exposure to these metals has been connected with increased risks of numerous cancers and as well as non-carcinogenic health outcomes, including cardiovascular disease, neurologic deficits, neuro-developmental deficits in childhood, and hypertension. However, currently the specific molecular targets for metal toxicity and carcinogenicity are not fully understood. Here, we propose that the iron- and 2-oxoglutarate-dependent dioxygenase family enzymes, as well as, other histone modifying enzymes are important intracellular targets that mediate the toxicity and carcinogenicity of nickel, and maybe potential targets in chromium and arsenic induced carcinogenesis. Our data demonstrate that all three metals are capable of inducing post-translational histone modifications and affecting the enzymes that modulate them (i.e. the iron- and 2-oxoglutarate-dependent dioxygenase family, including HIF-prolyl hydroxylase PHD2, histone demethylase JHDM2A/JMJD1A, and DNA repair enzymes ABH3 and ABH2, and histone methyltransferases, G9a). Given the effects that these metals can exert on the epigenome, future studies of their involvement in histone modifying enzymes dynamics would deepen our understanding on their respective toxicities and carcinogenicities.
MeSH term(s)	Animals ; Arsenic/toxicity ; Carcinogens/toxicity ; Chromium/toxicity ; Dioxygenases/metabolism ; Epigenomics ; Humans ; Nickel/toxicity
Chemical Substances	Carcinogens ; Chromium (0R0008Q3JB) ; Nickel (7OV03QG267) ; Dioxygenases (EC 1.13.11.-) ; Arsenic (N712M78A8G)
Language	English
Publishing date	2012-04-03
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2474317-3
ISSN	1756-591X ; 1756-5901
ISSN (online)	1756-591X
ISSN	1756-5901
DOI	10.1039/c2mt20033c
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Article ; Online: Craniofacial morphology of HIV-positive children and adolescents undergoing antiretroviral therapy: A pilot study.

Veloso de Almeida Watanabe, Maria Luiza / Oliveira Lira Ortega, Adriana / Riera Costa, Catalina / Saito Arita, Emiko / Ortega, Karem L

American journal of orthodontics and dentofacial orthopedics : official publication of the American Association of Orthodontists, its constituent societies, and the American Board of Orthodontics

2018 Volume 153, Issue 1, Page(s) 26–35

Abstract: Introduction: In this study, we aimed to analyze craniofacial morphology by assessing the skeletal cephalometric profiles of HIV-positive patients receiving antiretroviral therapy.: Methods: For this study, 21 HIV-positive patients aged between 6 and ...

Abstract	Introduction: In this study, we aimed to analyze craniofacial morphology by assessing the skeletal cephalometric profiles of HIV-positive patients receiving antiretroviral therapy. Methods: For this study, 21 HIV-positive patients aged between 6 and 17 years (study group) were selected and compared with 21 normoreactive patients (control group), paired by sex and age. The patients were also divided into 3 age ranges (6-8, 9-12, and 13-17 years) considering the pubertal growth spurt as the central event. Eighteen (linear and angular) measurements were traced on teleradiographs by using 2 methodologies. The mean values of each measurement were compared between the study and control groups by age range. Results: The majority of the measurements checked in the HIV-positive children and adolescents for the 13-to-17 year age range were diminished, but not enough to generate a statistically significant difference in craniofacial growth. Statistically significant differences (P <0.05) were found only in the inclination of the palatal plane (6-8 years) and the position of the maxilla in the anteroposterior direction (13-17 years). Conclusions: These results led us to conclude that some cephalometric measurements of HIV-positive children and adolescents may be similar to those of normoreactive subjects.
MeSH term(s)	Adolescent ; Antiretroviral Therapy, Highly Active ; Case-Control Studies ; Cephalometry ; Child ; Face/anatomy & histology ; Female ; HIV Seropositivity/drug therapy ; Humans ; Male ; Pilot Projects ; Skull/anatomy & histology
Language	English
Publishing date	2018-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	356699-7
ISSN	1097-6752 ; 0889-5406 ; 0002-9416
ISSN (online)	1097-6752
ISSN	0889-5406 ; 0002-9416
DOI	10.1016/j.ajodo.2017.05.027
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Article ; Online: Effects of nickel, chromate, and arsenite on histone 3 lysine methylation.

Zhou, Xue / Li, Qin / Arita, Adriana / Sun, Hong / Costa, Max

Toxicology and applied pharmacology

2009 Volume 236, Issue 1, Page(s) 78–84

Abstract: Occupational exposure to nickel (Ni), chromium (Cr), and arsenic (As) containing compounds has been associated with lung cancer and other adverse health effects. Their carcinogenic properties may be attributable in part, to activation and/or repression ... ...

Abstract	Occupational exposure to nickel (Ni), chromium (Cr), and arsenic (As) containing compounds has been associated with lung cancer and other adverse health effects. Their carcinogenic properties may be attributable in part, to activation and/or repression of gene expression induced by changes in the DNA methylation status and histone tail post-translational modifications. Here we show that individual treatment with nickel, chromate, and arsenite all affect the gene activating mark H3K4 methylation. We found that nickel (1 mM), chromate (10 microM), and arsenite (1 microM) significantly increase tri-methyl H3K4 after 24 h exposure in human lung carcinoma A549 cells. Seven days of exposure to lower levels of nickel (50 and 100 microM), chromate (0.5 and 1 microM) or arsenite (0.1, 0.5 and 1 microM) also increased tri-methylated H3K4 in A549 cells. This mark still remained elevated and inherited through cell division 7 days following removal of 1 microM arsenite. We also demonstrate by dual staining immunofluorescence microscopy that both H3K4 tri-methyl and H3K9 di-methyl marks increase globally after 24 h exposure to each metal treatment in A549 cells. However, the tri-methyl H3K4 and di-methyl H3K9 marks localize in different regions in the nucleus of the cell. Thus, our study provides further evidence that a mechanism(s) of carcinogenicity of nickel, chromate, and arsenite metal compounds may involve alterations of various histone tail modifications that may in turn affect the expression of genes that may cause transformation.
MeSH term(s)	Arsenites/toxicity ; Cell Line, Tumor ; Cell Transformation, Neoplastic/drug effects ; Chromates/toxicity ; Dose-Response Relationship, Drug ; Gene Expression Regulation, Neoplastic/drug effects ; Histones/metabolism ; Humans ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; Lysine ; Methylation ; Nickel/toxicity ; Potassium Compounds/toxicity ; Protein Processing, Post-Translational/drug effects ; Sodium Compounds/toxicity ; Time Factors
Chemical Substances	Arsenites ; Chromates ; Histones ; Potassium Compounds ; Sodium Compounds ; sodium arsenite (48OVY2OC72) ; nickel sulfate (4FLT4T3WUN) ; potassium chromate(VI) (5P0R38CN2X) ; nickel chloride (696BNE976J) ; Nickel (7OV03QG267) ; Lysine (K3Z4F929H6)
Language	English
Publishing date	2009-01-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	204477-8
ISSN	1096-0333 ; 0041-008X
ISSN (online)	1096-0333
ISSN	0041-008X
DOI	10.1016/j.taap.2009.01.009
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Article ; Online: Nuclear Factor κB1/RelA Mediates Inflammation in Human Lung Epithelial Cells at Atmospheric Oxygen Levels.

Jagannathan, Lakshmanan / Jose, Cynthia C / Arita, Adriana / Kluz, Thomas / Sun, Hong / Zhang, Xiaoru / Yao, Yixin / Kartashov, Andrey V / Barski, Artem / Costa, Max / Cuddapah, Suresh

Journal of cellular physiology

2016 Volume 231, Issue 7, Page(s) 1611–1620

Abstract: Oxygen levels range from 2% to 9% in vivo. Atmospheric O2 levels (21%) are known to induce cell proliferation defects and cellular senescence in primary cell cultures. However, the mechanistic basis of the deleterious effects of higher O2 levels is not ... ...

Abstract	Oxygen levels range from 2% to 9% in vivo. Atmospheric O2 levels (21%) are known to induce cell proliferation defects and cellular senescence in primary cell cultures. However, the mechanistic basis of the deleterious effects of higher O2 levels is not fully understood. On the other hand, immortalized cells including cancer cell lines, which evade cellular senescence are normally cultured at 21% O2 and the effects of higher O2 on these cells are understudied. Here, we addressed this problem by culturing immortalized human bronchial epithelial (BEAS-2B) cells at ambient atmospheric, 21% O2 and lower, 10% O2. Our results show increased inflammatory response at 21% O2 but not at 10% O2. We found higher RelA binding at the NF-κB1/RelA target gene promoters as well as upregulation of several pro-inflammatory cytokines in cells cultured at 21% O2. RelA knockdown prevented the upregulation of the pro-inflammatory cytokines at 21% O2, suggesting NF-κB1/RelA as a major mediator of inflammatory response in cells cultured at 21% O2. Interestingly, unlike the 21% O2 cultured cells, exposure of 10% O2 cultured cells to H2O2 did not elicit inflammatory response, suggesting increased ability to tolerate oxidative stress in cells cultured at lower O2 levels.
MeSH term(s)	Cell Proliferation ; Cellular Senescence ; Cytokines/genetics ; Cytokines/metabolism ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Gene Knockdown Techniques ; Humans ; Inflammation/metabolism ; Inflammation/pathology ; Lung/metabolism ; Lung/pathology ; Oxygen/metabolism ; Promoter Regions, Genetic ; Transcription Factor RelA/genetics ; Transcription Factor RelA/metabolism
Chemical Substances	Cytokines ; RELA protein, human ; Transcription Factor RelA ; Oxygen (S88TT14065)
Language	English
Publishing date	2016-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3116-1
ISSN	1097-4652 ; 0021-9541
ISSN (online)	1097-4652
ISSN	0021-9541
DOI	10.1002/jcp.25262
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Article ; Online: Signaling pathways in lymphoma: pathogenesis and therapeutic targets.

Arita, Adriana / McFarland, Daniel C / Myklebust, June H / Parekh, Samir / Petersen, Bruce / Gabrilove, Janice / Brody, Joshua D

Future oncology (London, England)

2013 Volume 9, Issue 10, Page(s) 1549–1571

Abstract: Lymphoma is the fifth most common cancer in the USA. Most lymphomas are classified as non-Hodgkin's lymphoma, and nearly 95% of these cancers are of B-cell origin. B-cell receptor (BCR) surface expression and BCR functional signaling are critical for ... ...

Abstract	Lymphoma is the fifth most common cancer in the USA. Most lymphomas are classified as non-Hodgkin's lymphoma, and nearly 95% of these cancers are of B-cell origin. B-cell receptor (BCR) surface expression and BCR functional signaling are critical for survival and proliferation of both healthy B cells, as well as most B-lymphoma cells. Agents that inhibit various components of the BCR signaling pathway, as well as parallel signaling pathways, are currently in clinical trials for the treatment of various lymphoma subtypes, including those targeting isoforms of PI3K, mTOR and BTK. In this review, we describe the signaling pathways in healthy mature B cells, the aberrant signaling in lymphomatous B cells and the rationale for clinical trials of agents targeting these pathways as well as the results of clinical trials to date. We propose that the entry into a kinase inhibitor era of lymphoma therapy will be as transformative for our patients as the advent of the antibody or chemotherapy era before it.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Humans ; Lymphoma/drug therapy ; Lymphoma/etiology ; Lymphoma/metabolism ; Molecular Targeted Therapy ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Signal Transduction/drug effects
Chemical Substances	Antineoplastic Agents ; Protein Kinase Inhibitors
Language	English
Publishing date	2013-10
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2184533-5
ISSN	1744-8301 ; 1479-6694
ISSN (online)	1744-8301
ISSN	1479-6694
DOI	10.2217/fon.13.113
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Article ; Online: Hypoxia induces trimethylated H3 lysine 4 by inhibition of JARID1A demethylase.

Zhou, Xue / Sun, Hong / Chen, Haobin / Zavadil, Jiri / Kluz, Thomas / Arita, Adriana / Costa, Max

Cancer research

2010 Volume 70, Issue 10, Page(s) 4214–4221

Abstract: Histone H3 lysine 4 (H3K4) trimethylation (H3K4me3) at the promoter region of genes has been linked to transcriptional activation. In the present study, we found that hypoxia (1% oxygen) increased H3K4me3 in both normal human bronchial epithelial Beas-2B ...

Abstract	Histone H3 lysine 4 (H3K4) trimethylation (H3K4me3) at the promoter region of genes has been linked to transcriptional activation. In the present study, we found that hypoxia (1% oxygen) increased H3K4me3 in both normal human bronchial epithelial Beas-2B cells and human lung carcinoma A549 cells. The increase of H3K4me3 from hypoxia was likely caused by the inhibition of H3K4 demethylating activity, as hypoxia still increased H3K4me3 in methionine-deficient medium. Furthermore, an in vitro histone demethylation assay showed that 1% oxygen decreased the activity of H3K4 demethylases in Beas-2B nuclear extracts because ambient oxygen tensions were required for the demethylation reaction to proceed. Hypoxia only minimally increased H3K4me3 in the BEAS-2B cells with knockdown of JARID1A, which is the major histone H3K4 demethylase in this cell line. However, the mRNA and protein levels of JARID1A were not affected by hypoxia. GeneChip and pathway analysis in JARID1A knockdown Beas-2B cells revealed that JARID1A regulates the expression of hundreds of genes involved in different cellular functions, including tumorigenesis. Knocking down of JARID1A increased H3K4me3 at the promoters of HMOX1 and DAF genes. Thus, these results indicate that hypoxia might target JARID1A activity, which in turn increases H3K4me3 at both the global and gene-specific levels, leading to the altered programs of gene expression and tumor progression.
MeSH term(s)	Biomarkers/metabolism ; Blotting, Western ; Bronchi/enzymology ; Bronchi/pathology ; Cells, Cultured ; Chromatin Immunoprecipitation ; DNA Methylation ; Epithelial Cells/enzymology ; Epithelial Cells/pathology ; Gene Expression Profiling ; Heme Oxygenase-1/genetics ; Heme Oxygenase-1/metabolism ; Histones/metabolism ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Lung Neoplasms/enzymology ; Lung Neoplasms/genetics ; Lung Neoplasms/pathology ; Lysine/genetics ; Lysine/metabolism ; Oligonucleotide Array Sequence Analysis ; Promoter Regions, Genetic/genetics ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; RNA, Small Interfering/pharmacology ; Retinoblastoma Protein/metabolism ; Retinoblastoma-Binding Protein 2/antagonists & inhibitors ; Retinoblastoma-Binding Protein 2/genetics ; Retinoblastoma-Binding Protein 2/metabolism ; Reverse Transcriptase Polymerase Chain Reaction
Chemical Substances	Biomarkers ; HIF1A protein, human ; Histones ; Hypoxia-Inducible Factor 1, alpha Subunit ; RNA, Messenger ; RNA, Small Interfering ; Retinoblastoma Protein ; KDM5A protein, human (EC 1.14.11.-) ; Retinoblastoma-Binding Protein 2 (EC 1.14.11.27) ; HMOX1 protein, human (EC 1.14.14.18) ; Heme Oxygenase-1 (EC 1.14.14.18) ; Lysine (K3Z4F929H6)
Language	English
Publishing date	2010-04-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-09-2942
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Article ; Online: The effect of exposure to carcinogenic metals on histone tail modifications and gene expression in human subjects.

Arita, Adriana / Shamy, Magdy Y / Chervona, Yana / Clancy, Harriet A / Sun, Hong / Hall, Megan N / Qu, Qingshan / Gamble, Mary V / Costa, Max

Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS)

2012 Volume 26, Issue 2-3, Page(s) 174–178

Abstract: The precise mechanisms by which nickel and arsenic compounds exert their carcinogenic properties are not completely understood. In recent years, alterations of epigenetic mechanisms have been implicated in the carcinogenesis of compounds of these two ... ...

Abstract	The precise mechanisms by which nickel and arsenic compounds exert their carcinogenic properties are not completely understood. In recent years, alterations of epigenetic mechanisms have been implicated in the carcinogenesis of compounds of these two metals. In vitro exposure to certain nickel or arsenic compounds induces changes in both DNA methylation patterns, as well as, in the levels of posttranslational modifications of histone tails. Changes in DNA methylation patterns have been reported in human subjects exposed to arsenic. Here we review our recent reports on the alterations in global levels of posttranslational histone modifications in peripheral blood mononuclear cells (PBMCs) of subjects with occupational exposure to nickel and subjects exposed to arsenic in their drinking water. Occupational exposure to nickel was associated with an increase in H3K4me3 and decrease in H3K9me2. A global increase in H3K9me2 and decrease in H3K9ac was found in subjects exposed to arsenic. Additionally, exposure to arsenic resulted in opposite changes in a number of histone modifications in males when compared with females in the arsenic population. The results of these two studies suggest that exposure to nickel or arsenic compounds, and possibly other carcinogenic metal compounds, can induce changes in global levels of posttranslational histone modifications in peripheral blood mononuclear cells.
MeSH term(s)	Arsenic/toxicity ; Carcinogens/toxicity ; Epigenesis, Genetic/drug effects ; Histones/drug effects ; Humans ; Nickel/toxicity
Chemical Substances	Carcinogens ; Histones ; Nickel (7OV03QG267) ; Arsenic (N712M78A8G)
Language	English
Publishing date	2012-05-24
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1236267-0
ISSN	1878-3252 ; 1611-602X ; 0946-672X
ISSN (online)	1878-3252 ; 1611-602X
ISSN	0946-672X
DOI	10.1016/j.jtemb.2012.03.012
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Article ; Online: Nickel compounds induce apoptosis in human bronchial epithelial Beas-2B cells by activation of c-Myc through ERK pathway.

Li, Qin / Suen, Ting-Chung / Sun, Hong / Arita, Adriana / Costa, Max

Toxicology and applied pharmacology

2008 Volume 235, Issue 2, Page(s) 191–198

Abstract: Nickel compounds are carcinogenic to humans and have been shown to alter epigenetic homeostasis. The c-Myc protein controls 15% of human genes and it has been shown that fluctuations of c-Myc protein alter global epigenetic marks. Therefore, the ... ...

Abstract	Nickel compounds are carcinogenic to humans and have been shown to alter epigenetic homeostasis. The c-Myc protein controls 15% of human genes and it has been shown that fluctuations of c-Myc protein alter global epigenetic marks. Therefore, the regulation of c-Myc by nickel ions in immortalized but not tumorigenic human bronchial epithelial Beas-2B cells was examined in this study. It was found that c-Myc protein expression was increased by nickel ions in non-tumorigenic Beas-2B and human keratinocyte HaCaT cells. The results also indicated that nickel ions induced apoptosis in Beas-2B cells. Knockout of c-Myc and its restoration in a rat cell system confirmed the essential role of c-Myc in nickel ion-induced apoptosis. Further studies in Beas-2B cells showed that nickel ion increased the c-Myc mRNA level and c-Myc promoter activity, but did not increase c-Myc mRNA and protein stability. Moreover, nickel ion upregulated c-Myc in Beas-2B cells through the MEK/ERK pathway. Collectively, the results demonstrate that c-Myc induction by nickel ions occurs via an ERK-dependent pathway and plays a crucial role in nickel-induced apoptosis in Beas-2B cells.
MeSH term(s)	Apoptosis/drug effects ; Blotting, Western ; Cell Line ; Epithelial Cells/drug effects ; Extracellular Signal-Regulated MAP Kinases/physiology ; Flow Cytometry ; Genes, Reporter ; Humans ; Keratinocytes/drug effects ; Luciferases/metabolism ; Nickel/toxicity ; Proto-Oncogene Proteins c-myc/physiology ; RNA/biosynthesis ; RNA/genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction/drug effects ; ras Proteins/genetics ; ras Proteins/physiology
Chemical Substances	Proto-Oncogene Proteins c-myc ; RNA (63231-63-0) ; Nickel (7OV03QG267) ; Luciferases (EC 1.13.12.-) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; ras Proteins (EC 3.6.5.2)
Language	English
Publishing date	2008-12-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	204477-8
ISSN	1096-0333 ; 0041-008X
ISSN (online)	1096-0333
ISSN	0041-008X
DOI	10.1016/j.taap.2008.12.005
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Article ; Online: Effects of nickel treatment on H3K4 trimethylation and gene expression.

Tchou-Wong, Kam-Meng / Kiok, Kathrin / Tang, Zuojian / Kluz, Thomas / Arita, Adriana / Smith, Phillip R / Brown, Stuart / Costa, Max

PloS one

2011 Volume 6, Issue 3, Page(s) e17728

Abstract: Occupational exposure to nickel compounds has been associated with lung and nasal cancers. We have previously shown that exposure of the human lung adenocarcinoma A549 cells to NiCl(2) for 24 hr significantly increased global levels of trimethylated H3K4 ...

Abstract	Occupational exposure to nickel compounds has been associated with lung and nasal cancers. We have previously shown that exposure of the human lung adenocarcinoma A549 cells to NiCl(2) for 24 hr significantly increased global levels of trimethylated H3K4 (H3K4me3), a transcriptional activating mark that maps to the promoters of transcribed genes. To further understand the potential epigenetic mechanism(s) underlying nickel carcinogenesis, we performed genome-wide mapping of H3K4me3 by chromatin immunoprecipitation and direct genome sequencing (ChIP-seq) and correlated with transcriptome genome-wide mapping of RNA transcripts by massive parallel sequencing of cDNA (RNA-seq). The effect of NiCl(2) treatment on H3K4me3 peaks within 5,000 bp of transcription start sites (TSSs) on a set of genes highly induced by nickel in both A549 cells and human peripheral blood mononuclear cells were analyzed. Nickel exposure increased the level of H3K4 trimethylation in both the promoters and coding regions of several genes including CA9 and NDRG1 that were increased in expression in A549 cells. We have also compared the extent of the H3K4 trimethylation in the absence and presence of formaldehyde crosslinking and observed that crosslinking of chromatin was required to observe H3K4 trimethylation in the coding regions immediately downstream of TSSs of some nickel-induced genes including ADM and IGFBP3. This is the first genome-wide mapping of trimethylated H3K4 in the promoter and coding regions of genes induced after exposure to NiCl(2). This study may provide insights into the epigenetic mechanism(s) underlying the carcinogenicity of nickel compounds.
MeSH term(s)	Antigens, Neoplasm/genetics ; Carbonic Anhydrase IX ; Carbonic Anhydrases/genetics ; Cell Cycle Proteins/genetics ; Cell Line, Tumor ; DNA Methylation/drug effects ; DNA Methylation/genetics ; Epigenesis, Genetic/drug effects ; Epigenesis, Genetic/genetics ; Histones/drug effects ; Histones/metabolism ; Humans ; Intracellular Signaling Peptides and Proteins/genetics ; Nickel/pharmacology
Chemical Substances	Antigens, Neoplasm ; Cell Cycle Proteins ; Histones ; Intracellular Signaling Peptides and Proteins ; N-myc downstream-regulated gene 1 protein ; Nickel (7OV03QG267) ; CA9 protein, human (EC 4.2.1.1) ; Carbonic Anhydrase IX (EC 4.2.1.1) ; Carbonic Anhydrases (EC 4.2.1.1)
Language	English
Publishing date	2011-03-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0017728
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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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