Luteolin Decreases Epidermal Growth Factor Receptor‐Mediated Cell Proliferation and Induces Apoptosis in Glioblastoma Cell Lines

Glioblastomas are a subtype of gliomas, which are the most aggressive and deadly form of brain tumours. The epidermal growth factor receptor (EGFR) is over‐expressed and amplified in glioblastomas. Luteolin is a common bioflavonoid found in a variety of fruits and vegetables. The aim of this study w...

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Bibliographic Details
Published in:Basic & clinical pharmacology & toxicology 2018-12, Vol.123 (6), p.678-686
Main Authors: Anson, David M., Wilcox, Rachel M., Huseman, Eric D., Stump, Trevor A., Paris, Robert L., Darkwah, Belinda O., Lin, Stacy, Adegoke, Andrea O., Gryka, Rebecca J., Jean‐Louis, Denise S., Amos, Samson
Format: Article
Language:English
Subjects:
AKT protein
Antineoplastic Agents - pharmacology
Apoptosis
Apoptosis - drug effects
Biological effects
Blotting, Western
Brain
Brain cancer
Brain tumors
Caspase
Cell cycle
Cell growth
Cell Line, Tumor
Cell lines
Cell proliferation
Cell Proliferation - drug effects
Epidermal growth factor
Epidermal growth factor receptors
ErbB Receptors - antagonists & inhibitors
Flow Cytometry
Glioblastoma
Glioblastoma - drug therapy
Glioblastoma cells
Growth factors
Humans
Luteolin - pharmacology
MAP kinase
Poly(ADP-ribose) polymerase
Proteins
Signal transduction
Signaling
TOR protein
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Summary:Glioblastomas are a subtype of gliomas, which are the most aggressive and deadly form of brain tumours. The epidermal growth factor receptor (EGFR) is over‐expressed and amplified in glioblastomas. Luteolin is a common bioflavonoid found in a variety of fruits and vegetables. The aim of this study was to explore the molecular and biological effects of luteolin on EGF‐induced cell proliferation and the potential of luteolin to induce apoptosis in glioblastoma cells. In vitro cell viability assays demonstrated that luteolin decreased cell proliferation in the presence or absence of EGF. Immunoblots revealed that luteolin decreased the protein expression levels of phosphorylated Akt, mTOR, p70S6K and MAPK in the presence of EGF. Furthermore, our results revealed the ability of luteolin to induce caspase and PARP cleavages in glioblastoma cells in addition to promoting cell cycle arrest. Our results demonstrated that luteolin has an inhibitory effect on downstream signalling molecules activated by EGFR, particularly the Akt and MAPK signalling pathways, and provided a rationale for further clinical investigation into the use of luteolin as a therapeutic molecule in the management of glioblastoma.
ISSN:1742-7835
1742-7843
DOI:10.1111/bcpt.13077