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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
Bibliographic description
| title: | Epidermal growth factor (EGF) augments the invasive potential of human glioblastoma multiforme cells via the activation of collaborative EGFR/ROS-dependent signaling |
| author: | Pudełe Maciej, Król Kamila, Catapano Jessica  , Wróbel Tomasz , Czyż Jarosław , Ryszawy Damian
|
| journal title: | International Journal of Molecular Sciences |
| volume: | 21 |
| issue: | 10 |
| date of publication : | 2020 |
| article ID: | 3605 |
| ISSN: |
1661-6596 |
| eISSN: |
1422-0067 |
| DOI: | |
| language: | English |
| journal language: | English |
| abstract in English: | 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. |
| keywords in English: | glioblastoma multiforme, epidermal growth factor, invasion, EGFR, ROS |
| affiliation: | Wydział Biochemii, Biofizyki i Biotechnologii : Zakład Biologii Komórki, Wydział Biochemii, Biofizyki i Biotechnologii |
| type: | journal article |
| subtype: | academic paper |
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Except where otherwise noted, this item's license is described as Udzielam licencji. Uznanie autorstwa 4.0 Międzynarodowa
Projekt „Repozytorium otwartego dostępu do dorobku naukowego i dydaktycznego UJ” współfinansowany w ramach poddziałania 2.3.1 „Cyfrowe udostępnianie zasobów nauki” Programu Operacyjnego Polska Cyfrowa z Europejskiego Funduszu Rozwoju Regionalnego i budżetu państwa na podstawie umowy o dofinansowanie nr POPC.02.03.01-00-0030/17-00
