NDLI: Trifolin induces apoptosis via extrinsic and intrinsic pathways in the NCI-H460 human non-small cell lung-cancer cell line.

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Trifolin induces apoptosis via extrinsic and intrinsic pathways in the NCI-H460 human non-small cell lung-cancer cell line.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Kim, Min-Je Kwon, Sae-Bom Kim, Man-Sub Jin, Seung Won Ryu, Hyung Won Oh, Sei-Ryang Yoon, Do-Young
Description	Author Affiliation: Kim MJ ( Department of Bioscience and Biotechnology, Bio/Molecular Informatics Center, Konkuk University, Gwangjin-gu, Seoul 05029, Republic of Korea.); Kwon SB ( Department of Bioscience and Biotechnology, Bio/Molecular Informatics Center, Konkuk University, Gwangjin-gu, Seoul 05029, Republic of Korea.); Kim MS ( Department of Bioscience and Biotechnology, Bio/Molecular Informatics Center, Konkuk University, Gwangjin-gu, Seoul 05029, Republic of Korea.); Jin SW ( Department of Bioscience and Biotechnology, Bio/Molecular Informatics Center, Konkuk University, Gwangjin-gu, Seoul 05029, Republic of Korea.); Ryu HW ( Natural Medicine Research Center, KRIBB, Cheongwon-gu, Cheongju-si, Republic of Korea.); Oh SR ( Natural Medicine Research Center, KRIBB, Cheongwon-gu, Cheongju-si, Republic of Korea.); Yoon DY ( Department of Bioscience and Biotechnology, Bio/Molecular Informatics Center, Konkuk University, Gwangjin-gu, Seoul 05029, Republic of Korea. Electronic address: ydy4218@hanmail.com.)
Abstract	BACKGROUND: Trifolin (kaempferol-3-O-galactoside), which is a galactose-conjugated flavonol, exhibits antifungal and anticancer effects. However, the mechanisms underlying its anticancer activities have not yet been examined. PURPOSE: In this study, the anticancer effects of trifolin were examined in human lung cancer cells. METHODS: Cytotoxicity was determined by evaluating cell viability. Apoptosis was analyzed through flow cytometry and western blotting analysis. Death receptors and inhibitors of apoptosis were evaluated through RT-PCR. RESULTS: Trifolin induced apoptosis in NCI-H460 human non-small cell lung cancer (NSCLC) cells by inhibiting the survival pathway and inducing the intrinsic and extrinsic apoptosis pathways. Trifolin decreased levels of Akt/p-Akt, whereas levels of expression of phosphatidylinositide 3-kinase (PI3K), cyclin D1, cyclin E, and cyclin A were not altered. Trifolin initiated cytochrome c release by inducing mitochondrial outer membrane permeabilization (MOMP). Trifolin increased Bcl-2-associated X protein (Bax) levels and decreased b-cell lymphoma 2 (Bcl-2) levels, while the levels of Bcl-xL were not altered. In addition, trifolin increased the levels of the death receptor involving the Fas/Fas ligand (FasL) and Fas-associated protein with the death domain (FADD), which consequently activated caspase-8, caspase-9, caspase-3, and the proteolytic cleavage of poly (ADP-ribose) polymerase (PARP). CONCLUSION: These results suggested that trifolin induced apoptosis via death receptor-dependent and mitochondria-dependent pathways and that trifolin can be used as a therapeutic agent in human lung cancer.
File Format	HTM / HTML
ISSN	09447113
Issue Number	10
Journal	Phytomedicine
Volume Number	23
e-ISSN	1618095X
Language	English
Publisher	Elsevier
Publisher Date	2016-09-15
Publisher Place	Germany
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Complementary Therapies
Content Type	Text
Resource Type	Article
Subject	Drug Discovery Molecular Medicine Pharmacology Complementary and Alternative Medicine Pharmaceutical Science

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