Hexachlorobenzene induces cell proliferation and IGF-I signaling pathway in an estrogen receptor α-dependent manner in MCF-7 breast cancer cell line

García, María Alejandra; Peña, Delfina; Álvarez, Laura; Cocca, Claudia; Pontillo, Carolina; Bergoc, Rosa; Pisarev, Diana Kleiman de; Randi, Andrea

doi:10.1016/j.toxlet.2009.10.026

Cited by 49 publications

(15 citation statements)

References 42 publications

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“…These metabolites or ROS generated as signaling molecules also lead to increased cell proliferation. García et al () found that environmental estrogens such as hexachlorobenzene (HCB) at low concentrations (0.005 and 0.05 μM) can increase cell proliferation in (ER+)MCF‐7 cells by activating nuclear ERα receptor signaling pathway, and higher concentrations of HCB can induce apoptotic effect on MCF‐7 cells and ultimately cause cell death. This result is similar with those of our study.…”

Section: Resultsmentioning

confidence: 99%

In vitro profiling of toxicity and endocrine disrupting effects of bisphenol analogues by employing MCF‐7 cells and two‐hybrid yeast bioassay

Lei

Peng

Wen

et al. 2016

Environmental Toxicology

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The potentially adverse health implications of bisphenol A (BPA) have led to increasing use of alternative bisphenols (BPs). However, little is known about the toxicity of alternative BPs. In this study, the cytotoxicity, genotoxicity, intracellular ROS formation, and Ca fluctuation effects of BPs on MCF-7 cells were evaluated. At the same time, the estrogenic and thyroidal hormone effect potentials of six BPs were also evaluated using two-hybrid yeast bioassay. The results showed that most BPs at 0.01-1 μM significantly increased cell viability in MCF-7 cells and at higher exposure concentrations of 25-100 μM, they caused a significant decrease of cell viability. At the same time, these BPs also at 25-100 μM significantly increased LDH release of MCF-7 cells. In addition, several BPs at 10-50 μM resulted in a significantly concentration-depended increase in DNA-damaging effect on MCF-7 cells and elevated ROS production. Most BPs at 0.0001-10 μM significantly increased intracellular Ca level. These results showed that bisphenol AF (BPAF) and thiodiphenol (TDP) exerted cell biological effect, estrogenic, and thyroidal effect potentials greater than those of BPA. The cytotoxicity and endocrine disrupting effects of other BPs are similar to or slightly lower than those of BPA. Therefore, as potential alternatives to BPA, endocrine disrupting effects and potential health harm of alternative BPs to human can also not be ignored. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 278-289, 2017.

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Section: Resultsmentioning

confidence: 99%

In vitro profiling of toxicity and endocrine disrupting effects of bisphenol analogues by employing MCF‐7 cells and two‐hybrid yeast bioassay

Lei

Peng

Wen

et al. 2016

Environmental Toxicology

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“…Src, also, is activated significantly after only 15 min of exposure of cells to TCDD (Figure 2b), in agreement with previous studies. 30,[33][34][35][36][37][38] The total amounts of FAK and Src remain constant during the course of those experiments.…”

Section: Ahr Activates Early Integrin Clusteringmentioning

confidence: 97%

The aryl hydrocarbon receptor regulates focal adhesion sites through a non-genomic FAK/Src pathway

Tomkiewicz

Herry

et al. 2012

Oncogene

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The aryl hydrocarbon receptor (AhR) is commonly described as a transcription factor, which regulates xenobiotic-metabolizing enzymes. Recent studies have suggested that the binding of ligands to the AhR also activates the Src kinase. In this manuscript, we show that the AhR, through the activation of Src, activates focal adhesion kinase (FAK) and promotes integrin clustering. These effects contribute to cell migration. Further, we show that the activation of the AhR increases the interaction of FAK with the metastatic marker, HEF1/NEDD9/CAS-L, and the expression of several integrins. Xenobiotic exposure, thus, may contribute to novel cell-migratory programs.

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“…Biological effects favouring malignant transformation were observed on human breast cells for: the pesticide hexachlorobenzene [154]; the organophosphorus pesticides malathion and parathion [155]; PCBs [156, 157]; bisphenol A [158, 159]; cadmium [160–162]; butyl benzyl phthalate [163]; organochlorine pesticides (p,p′-DDD plus p,p′-DDE plus o,p′-DDE plus aldrin plus dieldrin) [164]; cosmetics benzyl salicylate, benzyl benzoate and butylphenylmethylpropional (Lilial) [165]; nitrite [166]. …”

Section: Observations Indicating That Endocrine Disruptors Contribmentioning

confidence: 99%

Endocrine-Disrupting Chemicals: Associated Disorders and Mechanisms of Action

Coster

Larebeke

2012

Journal of Environmental and Public Health

456

295

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The incidence and/or prevalence of health problems associated with endocrine-disruption have increased. Many chemicals have endocrine-disrupting properties, including bisphenol A, some organochlorines, polybrominated flame retardants, perfluorinated substances, alkylphenols, phthalates, pesticides, polycyclic aromatic hydrocarbons, alkylphenols, solvents, and some household products including some cleaning products, air fresheners, hair dyes, cosmetics, and sunscreens. Even some metals were shown to have endocrine-disrupting properties. Many observations suggesting that endocrine disruptors do contribute to cancer, diabetes, obesity, the metabolic syndrome, and infertility are listed in this paper. An overview is presented of mechanisms contributing to endocrine disruption. Endocrine disruptors can act through classical nuclear receptors, but also through estrogen-related receptors, membrane-bound estrogen-receptors, and interaction with targets in the cytosol resulting in activation of the Src/Ras/Erk pathway or modulation of nitric oxide. In addition, changes in metabolism of endogenous hormones, cross-talk between genomic and nongenomic pathways, cross talk with estrogen receptors after binding on other receptors, interference with feedback regulation and neuroendocrine cells, changes in DNA methylation or histone modifications, and genomic instability by interference with the spindle figure can play a role. Also it was found that effects of receptor activation can differ in function of the ligand.

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Hexachlorobenzene induces cell proliferation and IGF-I signaling pathway in an estrogen receptor α-dependent manner in MCF-7 breast cancer cell line

Cited by 49 publications

References 42 publications

In vitro profiling of toxicity and endocrine disrupting effects of bisphenol analogues by employing MCF‐7 cells and two‐hybrid yeast bioassay

In vitro profiling of toxicity and endocrine disrupting effects of bisphenol analogues by employing MCF‐7 cells and two‐hybrid yeast bioassay

The aryl hydrocarbon receptor regulates focal adhesion sites through a non-genomic FAK/Src pathway

Endocrine-Disrupting Chemicals: Associated Disorders and Mechanisms of Action

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