Di-(2-ethylhexyl)phthalate (DEHP) increases Bcl-2/Bax ratio and modifies c-myc expression in Syrian hamster embryo (SHE) cells

Maire, Marie-Aline; Rast, C.; Vasseur, Paule

doi:10.1016/j.toxlet.2005.04.004

Cited by 26 publications

(13 citation statements)

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“…A low concentration of DEHP (0.001 mg/ml) induced deformities and heat shock protein gene expression changes in a larval aquatic macroinvertabrate [153]. In SHE cells, the in vitro concentration of DEHP reported to affect apoptosis [123] was greater than that for transformation. Limited studies of MEHP required larger concentrations for the same effects.…”

Section: Discussionmentioning

confidence: 92%

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DEHP: Genotoxicity and potential carcinogenic mechanisms—A review

Caldwell

2012

Mutation Research/Reviews in Mutation Research

193

101

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Section: Discussionmentioning

confidence: 92%

“…Along with transformation assays, SHE cells have been used to study the effects of DEHP on apoptosis. Growth factor deprivation induces apoptosis in SHE cells; as measured via fluorescence with concurrent changes in mRNA and protein expression of Bcl-2 and Bax, 24 h DEHP pretreatment (9.7 mg/ml) reversed this apoptosis [123].…”

Section: 233mentioning

confidence: 96%

DEHP: Genotoxicity and potential carcinogenic mechanisms—A review

Caldwell

2012

Mutation Research/Reviews in Mutation Research

193

101

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“…An interference with the cytokine TGF-β1 (transforming growth factor-β1) [24] or with TNF-α (tumor necrosis factor-α) has been described [25]. An increased level of Bcl-2 and negative regulation of c-Myc expression has been related to inhibition of apoptosis in Syrian hamster embryo cells treated with 50 μM of DEHP [26]. …”

Section: Introductionmentioning

confidence: 99%

Transcriptomic effects of di-(2-ethylhexyl)-phthalate in Syrian hamster embryo cells: an important role of early cytoskeleton disturbances in carcinogenesis?

Landkocz¹,

Poupin²,

Atienzar

et al. 2011

BMC Genomics

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BackgroundDi-(2-ethylhexyl)-phthalate (DEHP) is a commonly used plasticizer in polyvinylchloride (PVC) formulations and a potentially non-genotoxic carcinogen. The aim of this study was to identify genes whose level of expression is altered by DEHP by using a global wide-genome approach in Syrian hamster embryo (SHE) cells, a model similar to human cells regarding their responses to this type of carcinogen. With mRNA Differential Display (DD), we analysed the transcriptional regulation of SHE cells exposed to 0, 12.5, 25 and 50 μM of DEHP for 24 hrs, conditions which induced neoplastic transformation of these cells. A real-time quantitative polymerase chain reaction (qPCR) was used to confirm differential expression of genes identified by DD.ResultsGene expression profiling showed 178 differentially-expressed fragments corresponding to 122 genes after tblastx comparisons, 79 up-regulated and 43 down-regulated. The genes of interest were involved in many biological pathways, including signal transduction, regulation of the cytoskeleton, xenobiotic metabolism, apoptosis, lipidogenesis, protein conformation, transport and cell cycle. We then focused particularly on genes involved in the regulation of the cytoskeleton, one of the processes occurring during carcinogenesis and in the early steps of neoplastic transformation. Twenty one cytoskeleton-related genes were studied by qPCR. The down-regulated genes were involved in focal adhesion or cell junction. The up-regulated genes were involved in the regulation of the actin cytoskeleton and this would suggest a role of cellular plasticity in the mechanism of chemical carcinogenesis. The gene expression changes identified in the present study were PPAR-independent.ConclusionThis study identified a set of genes whose expression is altered by DEHP exposure in mammalian embryo cells. This is the first study that elucidates the genomic changes of DEHP involved in the organization of the cytoskeleton. The latter genes may be candidates as biomarkers predictive of early events in the multistep carcinogenic process.

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“…Inhibition of apoptosis in cultured human hepatocytes (Goll et al, 1999) and SHE cells (Maire et al, 2005;Pant et al, 2010) ERK activation as the consequence of atrazine binding to GPER (Albanito et al, 2015), aromatase induction (Albanito et al, 2015;Quignot et al, 2012;Sanderson et al, 2000) In vitro cell transformation assays (Perocco et al, 1995) …”

Section: Level 2/3mentioning

confidence: 99%