Aryl hydrocarbon receptor-associated genes in rat liver

Lindros, Kai O.; Oinonen, Teija; Kettunen, Eeva; Sippel, Helmuth; Muro-Lupori, Concha; Koivusalo, Martti

doi:10.1016/s0006-2952(97)00495-4

Cited by 31 publications

(11 citation statements)

References 27 publications

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“…It has been shown that RB1 increases activation of the AhR-Arnt complex in hepatoma cells [85] and this heterodimer complex is known to regulate CYP1B1 [86] and ALDH1 [87]. AhR has also been shown to decrease activation of phosphorylated E2F1 in tandem with RB1 [88,89].…”

Section: Resultsmentioning

confidence: 99%

Imprinted Genes and the Environment: Links to the Toxic Metals Arsenic, Cadmium and Lead

Smeester

Yosim

Nye

et al. 2014

Genes

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Imprinted genes defy rules of Mendelian genetics with their expression tied to the parent from whom each allele was inherited. They are known to play a role in various diseases/disorders including fetal growth disruption, lower birth weight, obesity, and cancer. There is increasing interest in understanding their influence on environmentally-induced disease. The environment can be thought of broadly as including chemicals present in air, water and soil, as well as food. According to the Agency for Toxic Substances and Disease Registry (ATSDR), some of the highest ranking environmental chemicals of concern include metals/metalloids such as arsenic, cadmium, and lead. The complex relationships between toxic metal exposure, imprinted gene regulation/expression and health outcomes are understudied. Herein we examine trends in imprinted gene biology, including an assessment of the imprinted genes and their known functional roles in the cell, particularly as they relate to toxic metals exposure and disease. The data highlight that many of the imprinted genes have known associations to developmental diseases and are enriched for their role in the TP53 and AhR pathways. Assessment of the promoter regions of the imprinted genes resulted in the identification of an enrichment of binding sites for two transcription factor families, namely the zinc finger family II and PLAG transcription factors. Taken together these data contribute insight into the complex relationships between toxic metals in the environment and imprinted gene biology.

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Section: Resultsmentioning

confidence: 99%

Imprinted Genes and the Environment: Links to the Toxic Metals Arsenic, Cadmium and Lead

Smeester

Yosim

Nye

et al. 2014

Genes

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“…The cholesterol oxidation product 7-ketocholesterol is a ligand for AhR and may function as an AhR antagonist (Savouret et al , 2001). Aryl hydrocarbon receptor pathway has been suggested to have an essential role in detoxification of foreign chemicals and in the protection against oxidative stress by increasing the expression of ALDH proteins (Lindros et al , 1998; Nebert et al , 2000; Vrzal et al , 2004; Kohle and Bock, 2007). Moreover, AhR is overexpressed in prostate cancer and cancer stem cells and it can bind to NF- κ B and promote activation of MYC (Kim et al , 2000; Blum et al , 2009; Gluschnaider et al , 2010).…”

Section: Discussionmentioning

confidence: 99%

Salinomycin inhibits prostate cancer growth and migration via induction of oxidative stress

et al. 2012

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Background:We have shown that a sodium ionophore monensin inhibits prostate cancer cell growth. A structurally related compound to monensin, salinomycin, was recently identified as a putative cancer stem cell inhibitor.Methods:The growth inhibitory potential of salinomycin was studied in a panel of prostate cells. To get insights into the mechanism of action, a variety of assays such as gene expression and steroid profiling were performed in salinomycin-exposed prostate cancer cells.Results:Salinomycin inhibited the growth of prostate cancer cells, but did not affect non-malignant prostate epithelial cells. Salinomycin impacted on prostate cancer stem cell functions as evidenced by reduced aldehyde dehydrogenase activity and the fraction of CD44+ cells. Moreover, salinomycin reduced the expression of MYC, AR and ERG, induced oxidative stress as well as inhibited nuclear factor-κB activity and cell migration. Furthermore, profiling steroid metabolites revealed increased levels of oxidative stress-inducing steroids 7-ketocholesterol and aldosterone and decreased levels of antioxidative steroids progesterone and pregnenolone in salinomycin-exposed prostate cancer cells.Conclusion:Our results indicate that salinomycin inhibits prostate cancer cell growth and migration by reducing the expression of key prostate cancer oncogenes, inducing oxidative stress, decreasing the antioxidative capacity and cancer stem cell fraction.

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“…The pink area indicates the relative abundance of the proteins along the sinusoids, from the periportally most proximal cells (p) to the most distal ones surrounding the terminal hepatic vein (v), as analysed from periportal and perivenous cell lysates. The Figure is compiled from data presented in [121], [195] and [199].…”

Section: Figure 7 Schematic Comparison Of the Influence Of 3mc Or Bnfmentioning

confidence: 99%

“…resembling those on CYP1A1\2, have been observed on the induction of GSTYa and ALDH3. Whereas MC induced these gene products exclusively in the perivenous region, BNF also caused substantial induction in the periportal cells [195]. This suggests that the common perivenous constitutive expression of these genes [2] and their similar inducer-specific zonation pattern are features characteristic for the members of the Ah gene battery.…”

Section: Figure 7 Schematic Comparison Of the Influence Of 3mc Or Bnfmentioning

confidence: 99%

Zonation of hepatic cytochrome P-450 expression and regulation

Oinonen

Lindros

1998

Biochemical Journal

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199

140

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The CYP genes encode enzymes of the cytochrome P-450 superfamily. Cytochrome P-450 (CYP) enzymes are expressed mainly in the liver and are active in mono-oxygenation and hydroxylation of various xenobiotics, including drugs and alcohols, as well as that of endogenous compounds such as steroids, bile acids, prostaglandins, leukotrienes and biogenic amines. In the liver the CYP enzymes are constitutively expressed and commonly also induced by chemicals in a characteristic zonated pattern with high expression prevailing in the downstream perivenous region. In the present review we summarize recent studies, mainly based on rat liver, on the factors regulating this position-dependent expression and induction. Pituitary-dependent signals mediated by growth hormone and thyroid hormone seem to selectively down-regulate the upstream periportal expression of certain CYP forms. It is at present unknown to what extent other hormones that also affect total hepatic CYP activities, i.e. insulin, glucagon, glucocorticoids and gonadal hormones, act zone-specifically. The expression and induction of CYP enzymes in the perivenous region probably have important toxicological implications, since many CYP-activated chemicals cause cell injury primarily in this region of the liver.

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Aryl hydrocarbon receptor-associated genes in rat liver

Cited by 31 publications

References 27 publications

Imprinted Genes and the Environment: Links to the Toxic Metals Arsenic, Cadmium and Lead

Imprinted Genes and the Environment: Links to the Toxic Metals Arsenic, Cadmium and Lead

Salinomycin inhibits prostate cancer growth and migration via induction of oxidative stress

Zonation of hepatic cytochrome P-450 expression and regulation

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