학술논문
Arctigenin induces caspase-dependent apoptosis in FaDu human pharyngeal carcinoma cells
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- 영문명
- Arctigenin induces caspase-dependent apoptosis in FaDu human pharyngeal carcinoma cells
- 발행기관
- 대한생리학회-대한약리학회
- 저자명
- Kyeong-Rok Kang Jae-Sung Kim HyangI Lim Jeong-Yeon Seo Jong-Hyun Park Hong Sung Chun Sun-Kyoung Yu
- 간행물 정보
- 『The Korean Journal of Physiology & Pharmacology』제26권 제6호, 447~456쪽, 전체 10쪽
- 주제분류
- 의약학 > 의학일반
- 파일형태
- 발행일자
- 2022.11.30
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국문 초록
영문 초록
The present study was carried out to investigate the effect of Arctigenin on cell growth and the mechanism of cell death elicited by Arctigenin were examined in FaDu human pharyngeal carcinoma cells. To determine the apoptotic activity of Arctigenin in FaDu human pharyngeal carcinoma cells, cell viability assay, DAPI staining, caspase activation analysis, and immunoblotting were performed. Arctigenin inhibited the growth of cells in a dose-dependent manner and induced nuclear condensation and fragmentation. Arctigenin-treated cells showed caspase-3/7 activation and increased apoptosis versus control cells. FasL, a death ligand associated with extrinsic apoptotic signaling pathways, was up-regulated by Arctigenin treatment. Moreover, caspase-8, a part of the extrinsic apoptotic pathway, was activated by Arctigenin treatments. Expressions of anti-apoptotic factors such as Bcl-2 and Bcl-xL, components of the mitochondria-dependent intrinsic apoptosis pathway, significantly decreased following Arctigenin treatment. The expressions of pro-apoptotic factors such as BAX, BAD and caspase-9, and tumor suppressor -53 increased by Arctigenin treatments. In addition, Arctigenin activated caspase-3 and poly (ADP-ribose) polymerase (PARP) induced cell death. Arctigenin also inhibited the proliferation of FaDu cells by the suppression of p38, NF-κB, and Akt signaling pathways. These results suggest that Arctigenin may inhibit cell proliferation and induce apoptotic cell death in FaDu human pharyngeal carcinoma cells through both the mitochondria-mediated intrinsic pathway and the death receptormediated extrinsic pathway.
목차
INTRODUCTION
METHODS
RESULTS
DISCUSSION
FUNDING
ACKNOWLEDGEMENTS
CONFLICTS OF INTEREST
REFERENCES
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