The cooked meat-derived mammary carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) elicits estrogenic-like microRNA responses in breast cancer cells

Papaioannou, Michael D.; Koufaris, Costas; Gooderham, Nigel J.

doi:10.1016/j.toxlet.2014.05.021

Cited by 27 publications

(16 citation statements)

References 58 publications

(75 reference statements)

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“…grilling on a charcoal grill, results in the formation of heterocyclic amines (HCA), including the most abundant: 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) which is considered a mammary carcinogen ( 177 ). Treatment of MCF-7 cells with 100 nM PhIP decreased miR-21, miR-1, and miR-106b expression and increased miR-923, miR-574-3p, miR-574-5p, and miR-494 ( 160 ). Other miRNAs regulated by PhIP are listed in Tables 1 and 2 .…”

Section: Endocrine Disrupting Chemicals Regulating Mirna Expressimentioning

confidence: 99%

miRNAs regulated by estrogens, tamoxifen, and endocrine disruptors and their downstream gene targets

Klinge

2015

Molecular and Cellular Endocrinology

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MicroRNAs (miRNAs) are short (22 nucleotides), single-stranded, non-coding RNAs that form complimentary base-pairs with the 3’ untranslated region of target mRNAs within the RNA-induced silencing complex (RISC) and block translation and/or stimulate mRNA transcript degradation. The non-coding miRBase (release 21, June 2014) reports that human genome contains ~2,588 mature miRNAs which regulate ~ 60% of human protein-coding mRNAs. Dysregulation of miRNA expression has been implicated in estrogen-related diseases including breast and endometrial cancers. The mechanism for estrogen regulation of miRNA expression and the role of estrogen-regulated miRNAs in normal homeostasis, reproduction, lactation, and in cancer is an area of great research and clinical interest. Estrogens regulate miRNAs transcription through estrogen receptors α and β in a tissue-specific and cell-dependent manner. This review focuses primary on the regulation of miRNA expression by ligand-activated ERs and their bona fide gene targets and includes miRNAs regulation by tamoxifen and endocrine disrupting chemicals (EDCs) in breast cancer and cell lines.

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Section: Endocrine Disrupting Chemicals Regulating Mirna Expressimentioning

confidence: 99%

miRNAs regulated by estrogens, tamoxifen, and endocrine disruptors and their downstream gene targets

Klinge

2015

Molecular and Cellular Endocrinology

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“…MiR‐638 was identified as a two‐hit oncogenic locus that targets both p53 and PTEN in multiple cancers . Expression of miR‐638 was also associated with carcinogenic treatments, having being reported to be affected by 2‐amino‐1‐methyl‐6‐phenylimidazo[4,5‐b]pyridine (PhIP) treatment in breast cancer cells . Furthermore, it contributes to benzo(a) pyrene (BaP) transformation of cancer cells .…”

Section: Hsm and Psm Are Reported To Act As Oncogenesmentioning

confidence: 99%

Human and primate‐specific microRNAs in cancer: Evolution, and significance in comparison with more distantly‐related research models

Koufaris

2016

BioEssays

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The largest proportion of microRNAs in humans (ca. 40-50%) originated in the phylogenetic grouping defined as primates. The dynamic evolution of this family of non-coding RNA is further demonstrated by the presence of microRNA unique to the human species. Investigations into the role of microRNA in cancer have until recently mainly focused on the more ancient members of this RNA family that are widely conserved in the animal kingdom. As I describe in this review the evolutionary young lineage and species-specific microRNA could be important contributors to cancers, especially in particular organs in primates compared to more distantly-related research models. Elucidating the biological significance of primate and human-specific microRNA in cancer could have important implications for cancer research and the use of non-primate animal models.

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“…It has also been shown that environmental agents such as pollution, cigarette smoke and food-derived carcinogens can influence the expression of miRNAs (Sonkoly and Pivarcsi 2011 ) associated with phenotype dysregulation and pathology. The use of miRNA profiles as an indicator of response to carcinogenic toxicants has been investigated (Gooderham and Koufaris 2014 ; Koufaris et al 2012 ; Papaioannou et al 2014 ).…”

Section: Introductionmentioning

confidence: 99%

Mechanistic evidence that benzo[a]pyrene promotes an inflammatory microenvironment that drives the metastatic potential of human mammary cells

2018

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Benzo[a]pyrene (B(a)P) is a major cancer-causing contaminant present in food such as cooked meats and cereals, and is ubiquitous in the environment in smoke derived from the combustion of organic material. Exposure to B(a)P is epidemiologically linked with the incidence of breast cancer. Although B(a)P is recognized as a complete genotoxic carcinogen, thought to act primarily via CYP-mediated metabolic activation to DNA-damaging species, there is also evidence that B(a)P exposure elicits other biological responses that promote development of the cancer phenotype. Here in mechanistic studies using human mammary cells MCF-7 and MDA-MB-231, we have explored mechanisms whereby B(a)P (10− 8 to 10− 5M) promotes inflammation pathways via TNF-α and NFκB leading to IL-6 upregulation, microRNA (Let7a, miR21 and miR29b) dysregulation and activation of VEGF. The miRNA dysregulation is associated with altered expression of inflammation mediators and increased migration and invasive potential of human mammary cancer cells. Our data suggest that mammary cell exposure to B(a)P results in perturbation of inflammation mediators and dysregulation of tumorigenic miRNAs, leading to an inflammation microenvironment that facilitates migration and invasion of mammary epithelial cells. These properties of B(a)P, together with its well-established metabolic activation to DNA-damaging species, offer mechanistic insights into its carcinogenic mode of action.

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The cooked meat-derived mammary carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) elicits estrogenic-like microRNA responses in breast cancer cells

Cited by 27 publications

References 58 publications

miRNAs regulated by estrogens, tamoxifen, and endocrine disruptors and their downstream gene targets

miRNAs regulated by estrogens, tamoxifen, and endocrine disruptors and their downstream gene targets

Human and primate‐specific microRNAs in cancer: Evolution, and significance in comparison with more distantly‐related research models

Mechanistic evidence that benzo[a]pyrene promotes an inflammatory microenvironment that drives the metastatic potential of human mammary cells

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