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Luteolin Decreases Epidermal Growth Factor Receptor‐Mediated Cell Proliferation and Induces Apoptosis in Glioblastoma Cell Lines
Author(s) -
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.,
JeanLouis Denise S.,
Amos Samson
Publication year - 2018
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/bcpt.13077
Subject(s) - luteolin , mapk/erk pathway , cell growth , pi3k/akt/mtor pathway , apoptosis , cancer research , epidermal growth factor , epidermal growth factor receptor , protein kinase b , microbiology and biotechnology , cell , biology , chemistry , signal transduction , receptor , biochemistry , flavonoid , antioxidant
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.