High bisphenol A concentrations augment the invasiveness of tumor cells through Snail-1/Cx43/ERRγ-dependent epithelial-mesenchymal transition

Ryszawy, Damian; Pudełek, Maciej; Kochanowski, Paweł; Janik-Olchawa, Natalia; Bogusz, J; Rąpała, Michał; Koczurkiewicz, Paulina; Mikołajczyk, Justyna; Borek, Izabela; Kędracka–Krok, Sylwia; Karnas, Elżbieta; Zuba‐Surma, Ewa; Madeja, Zbigniew; Czyż, Jarosław

doi:10.1016/j.tiv.2019.104676

Cited by 15 publications

(16 citation statements)

References 53 publications

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“…The viability of the cells was estimated with a Trypan blue (Sigma; No. T8154) assay using a Burker hemocytometer, as described previously [44]. An MTT assay was applied to estimate the changes in relative cellular metabolic activity.…”

Section: Cell Proliferation Viability and Mtt Assaysmentioning

confidence: 99%

Epidermal Growth Factor (EGF) Augments the Invasive Potential of Human Glioblastoma Multiforme Cells via the Activation of Collaborative EGFR/ROS-Dependent Signaling

Pudełek

Krol

Catapano

et al. 2020

IJMS

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Abnormal secretion of epidermal growth factor (EGF) by non-neuronal cells (e.g., glioma-associated microglia) establishes a feedback loop between glioblastoma multiforme (GBM) invasion and a functional disruption of brain tissue. Considering the postulated significance of this vicious circle for GBM progression, we scrutinized mechanisms of EGF-dependent pro-invasive signaling in terms of its interrelations with energy metabolism and reactive oxygen species (ROS) production. The effects of EGF on the invasiveness of human glioblastoma T98G cells were estimated using time-lapse video microscopy, immunocytochemistry, cell cycle assay, immunoblot analyses, and Transwell® assay. These techniques were followed by quantification of the effect of EGFR (Epidermal Growth Factor Receptor) and ROS inhibitors on the EGF-induced T98G invasiveness and intracellular ROS, ATP, and lactate levels and mitochondrial metabolism. The EGF remarkably augmented the proliferation and motility of the T98G cells. Responses of these cells were accompanied by cellular rear–front polarization, translocation of vinculin to the leading lamellae, and increased promptness of penetration of micropore barriers. Erlotinib (the EGFR inhibitor) significantly attenuated the EGF-induced T98G invasiveness and metabolic reprogramming of the T98G cells, otherwise illustrated by the increased mitochondrial activity, glycolysis, and ROS production in the EGF-treated cells. In turn, ROS inhibition by N-acetyl-L-cysteine (NAC) had no effect on T98G morphology, but considerably attenuated EGF-induced cell motility. Our data confirmed the EGFR/ROS-dependent pro-neoplastic and pro-invasive activity of EGF in human GBM. These EGF effects may depend on metabolic reprogramming of GBM cells and are executed by alternative ROS-dependent/-independent pathways. The EGF may thus preserve bioenergetic homeostasis of GBM cells in hypoxic regions of brain tissue.

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Section: Cell Proliferation Viability and Mtt Assaysmentioning

confidence: 99%

Epidermal Growth Factor (EGF) Augments the Invasive Potential of Human Glioblastoma Multiforme Cells via the Activation of Collaborative EGFR/ROS-Dependent Signaling

Pudełek

Krol

Catapano

et al. 2020

IJMS

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“…Cell movement was registered 24, 48 and 72 h after administration of tested forms of Fe, for 8 h with 5 min intervals using Leica DMI6000B microscope equipped with a IMC contrast optics, DFC360FX CCD camera and chamber allowing the control of CO 2 level and temperature. Average parameters of cell movement, namely average speed of cell movement (µm/min) and distance (µm) were quantified from the trajectories of 50 cells in each condition using Hiro program written by Czapla as described in the paper of Ryszawy et al 73 .…”

Section: Methodsmentioning

confidence: 99%

Comparison of ultrasmall IONPs and Fe salts biocompatibility and activity in multi-cellular in vitro models

Janik-Olchawa

Dróżdż

Ryszawy

et al. 2020

Sci Rep

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In the paper, the results of the first regular studies of ultra-small iron oxide nanoparticles (IONPs) toxicity in vitro were presented. The influence of PEG-coated NPs with 5 nm magnetite core on six different cell lines was examined. These were: human bronchial fibroblasts, human embryonic kidney cells (HEK293T), two glioblastoma multiforme (GBM) cell lines as well as GBM cells isolated from a brain tumor of patient. Additionally, mouse macrophages were included in the study. The influence of IONPs in three different doses (1, 5 and 25 µg Fe/ml) on the viability, proliferation and migration activity of cells was assessed. Moreover, quantifying the intracellular ROS production, we determined the level of oxidative stress in cells exposed to IONPs. In the paper, for the first time, the effect of Fe in the form of IONPs was compared with the analogical data obtained for iron salts solutions containing the same amount of Fe, on the similar oxidation state. Our results clearly showed that the influence of iron on the living cells strongly depends not only on the used cell line, dose and exposure time but also on the form in which this element was administered to the culture. Notably, nanoparticles can stimulate the proliferation of some cell lines, including glioblastoma multiforme. Compared to Fe salts, they have a stronger negative impact on the viability of the cells tested. Ultra-small NPs, also, more often positively affect cell motility which seem to differ them from the NPs with larger core diameters.

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“…ERK1 and MMPs activation are potential procarcinogenic signals in numerous cancers, including LC. Similarly, another study involving the cross talk between BPA and induction of pro-metastatic signaling suggested the activation of SNAI1/Cx43/ERRγ-dependent EMT signaling pathway upon BPA exposure in A549 cells (Ryszawy et al 2019). BPA induces morphological changes and enhances motility by cytoskeletal rearrangements (Zhang et al 2014).…”

Section: Lung Cancermentioning

confidence: 96%

“…BPA induces morphological changes and enhances motility by cytoskeletal rearrangements (Zhang et al 2014 ). Some studies reported BPA to induce EMT in lung cancer via a switch from CDH1 to CDH2 and vimentin/ SNAI 1/connexin (Cx) 43 upregulation (Ryszawy et al 2019 ). Besides inducing migration and invasion, BPA exposure is responsible for the inflammation and oxidative stress in rat lung tissues.…”

Section: Lung Cancermentioning

confidence: 99%

A comprehensive review on the carcinogenic potential of bisphenol A: clues and evidence

Khan

Correia

Adiga

et al. 2021

Environ Sci Pollut Res

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Bisphenol A [BPA; (CH3)2C(C6H4OH)2] is a synthetic chemical used as a precursor material for the manufacturing of plastics and resins. It gained attention due to its high chances of human exposure and predisposing individuals at extremely low doses to diseases, including cancer. It enters the human body via oral, inhaled, and dermal routes as leach-out products. BPA may be anticipated as a probable human carcinogen. Studies using in vitro cell lines, rodent models, and epidemiological analysis have convincingly shown the increasing susceptibility to cancer at doses below the oral reference dose set by the Environmental Protection Agency for BPA. Furthermore, BPA exerts its toxicological effects at the genetic and epigenetic levels, influencing various cell signaling pathways. The present review summarizes the available data on BPA and its potential impact on cancer and its clinical outcome.

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High bisphenol A concentrations augment the invasiveness of tumor cells through Snail-1/Cx43/ERRγ-dependent epithelial-mesenchymal transition

Cited by 15 publications

References 53 publications

Epidermal Growth Factor (EGF) Augments the Invasive Potential of Human Glioblastoma Multiforme Cells via the Activation of Collaborative EGFR/ROS-Dependent Signaling

Epidermal Growth Factor (EGF) Augments the Invasive Potential of Human Glioblastoma Multiforme Cells via the Activation of Collaborative EGFR/ROS-Dependent Signaling

Comparison of ultrasmall IONPs and Fe salts biocompatibility and activity in multi-cellular in vitro models

A comprehensive review on the carcinogenic potential of bisphenol A: clues and evidence

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