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Epidermal growth factor (EGF) augments the invasive potential of human glioblastoma multiforme cells via the activation of collaborative EGFR/ROS-dependent signaling

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Epidermal growth factor (EGF) augments the invasive potential of human glioblastoma multiforme cells via the activation of collaborative EGFR/ROS-dependent signaling

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dc.contributor.author Pudełe, Maciej pl
dc.contributor.author Król, Kamila pl
dc.contributor.author Catapano, Jessica [USOS150721] pl
dc.contributor.author Wróbel, Tomasz [USOS149880] pl
dc.contributor.author Czyż, Jarosław [SAP11015316] pl
dc.contributor.author Ryszawy, Damian [SAP14007358] pl
dc.date.accessioned 2020-11-07T15:49:28Z
dc.date.available 2020-11-07T15:49:28Z
dc.date.issued 2020 pl
dc.identifier.issn 1661-6596 pl
dc.identifier.uri https://ruj.uj.edu.pl/xmlui/handle/item/252941
dc.language eng pl
dc.rights Udzielam licencji. Uznanie autorstwa 4.0 Międzynarodowa *
dc.rights.uri http://creativecommons.org/licenses/by/4.0/pl/legalcode *
dc.title Epidermal growth factor (EGF) augments the invasive potential of human glioblastoma multiforme cells via the activation of collaborative EGFR/ROS-dependent signaling pl
dc.type JournalArticle pl
dc.abstract.en Abnormal secretion of epidermal growth factor (EGF) by non-neuronal cells (e.g., gliomaassociated 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. pl
dc.subject.en glioblastoma multiforme pl
dc.subject.en epidermal growth factor pl
dc.subject.en invasion pl
dc.subject.en EGFR pl
dc.subject.en ROS pl
dc.description.volume 21 pl
dc.description.number 10 pl
dc.identifier.doi 10.3390/ijms21103605 pl
dc.identifier.eissn 1422-0067 pl
dc.title.journal International Journal of Molecular Sciences pl
dc.language.container eng pl
dc.affiliation Wydział Biochemii, Biofizyki i Biotechnologii : Zakład Biologii Komórki pl
dc.affiliation Wydział Biochemii, Biofizyki i Biotechnologii pl
dc.subtype Article pl
dc.identifier.articleid 3605 pl
dc.rights.original CC-BY; otwarte czasopismo; ostateczna wersja wydawcy; w momencie opublikowania; 0 pl
dc.identifier.project ROD UJ / OP pl
.pointsMNiSW [2020 A]: 140


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Udzielam licencji. Uznanie autorstwa 4.0 Międzynarodowa Except where otherwise noted, this item's license is described as Udzielam licencji. Uznanie autorstwa 4.0 Międzynarodowa