Quercetin induces cell death by caspase-dependent and p38 MAPK pathway in EGFR mutant lung cancer cells.
- Author:
Eun Jin LIM
1
;
Jeunghoon HEO
;
Young Ho KIM
Author Information
- Publication Type:Original Article
- Keywords: EGFR mutant; Lung cancer; MAPK; Mitochondria; Quercetin
- MeSH: Apoptosis; Blotting, Western; Cell Death*; Cytochromes c; DNA Fragmentation; Lung Neoplasms*; Lung*; Mitochondria; p38 Mitogen-Activated Protein Kinases*; Quercetin*; Rotenone
- From:Kosin Medical Journal 2016;31(1):30-40
- CountryRepublic of Korea
- Language:English
- Abstract: OBJECTIVES: The aim of this study was whether quercetin induces cell death by caspase and MAPK signaling pathway in EGFR mutant lung cancer cells. METHODS: PC-9 cells, EGFR mutant lung cancer cells, were treated various times and concentrations of quercetin and harvested and measured using MTT assay, DNA fragmentation, Western blotting, and FACS analysis. RESULTS: Treatment with quercetin in PC-9 cells resulted in inhibition of cell growth through apoptosis. Quercetin-induced apoptosis was associated with caspase-dependent manner. Quercetin also significantly increased levels of phosphor-p38 and decreased levels of phosphor-ERK, indicating that quercetin induces p38 MAPK signaling pathway in PC-9 cells. Quecetin treatment also generated the release of cytochrome c in PC-9 cells; however, pretreatment with rotenone or z-LEHD-fmk, significantly attenuated quercetin-induced apoptosis. CONCLUSIONS: Our data indicate that quercetin exhibits EGFR mutant lung cancer effects through apoptosis by caspase dependent and mitochondrial pathway.
