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논문 기본 정보

자료유형
학술저널
저자정보
Kang Kyeong-Rok (The Institute of Dental Science Chosun University Gwangju 61452 Korea) Kim Jae-Sung (The Institute of Dental Science Chosun University Gwangju 61452 Korea) Lim HyangI (The Institute of Dental Science Chosun University Gwangju 61452 Korea) Seo Jeong-Yeon (The Institute of Dental Science Chosun University Gwangju 61452 Korea) Park Jong-Hyun (The Institute of Dental Science Chosun University Gwangju 61452 Korea) Chun Hong Sung (Department of Integrative Biological Sciences) Yu Sun-Kyoung (The Institute of Dental Science Chosun University Gwangju 61452 Korea) Kim Heung-Joong (The Institute of Dental Science Chosun University Gwangju 61452 Korea) Kim Chun Sung (The Institute of Dental Science Chosun University Gwangju 61452 Korea) 김도경 (조선대학교)
저널정보
대한약리학회 The Korean Journal of Physiology & Pharmacology The Korean Journal of Physiology & Pharmacology 제26권 제6호
발행연도
2022.11
수록면
447 - 456 (10page)
DOI
10.4196/kjpp.2022.26.6.447

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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. INTRODUCTION Head and neck cancers such as oral cancer, pharyngeal cancer, and laryngeal cancer are the most common cancers worldwide, especially in South America, Asia, and Europe [1-3]. Also, most of them are squamous cell carcinoma [4]. In the last 30 years, the survival rate of head and neck cancer has not improved significantly despite modern medical techniques and treatments such as the use of anticancer drugs [3,5]. Clinical treatment for head and neck cancer may induce adverse effects related to functional changes
#Apoptosis #Arctigenin #Caspase-dependent #Human pharyngeal carcinoma

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