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  4. Apoptotic effects of extract from Antrodia camphorata fruiting bodies in human hepatocellular carcinoma cell lines
 
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Apoptotic effects of extract from Antrodia camphorata fruiting bodies in human hepatocellular carcinoma cell lines

Journal
Cancer Letters
Journal Volume
221
Journal Volume
221
Journal Issue
1
Journal Issue
1
Pages
77-89
Start Page
77
End Page
89
ISSN
03043835
Date Issued
2005-04-18
Author(s)
Hsu, Ya-Ling
Kuo, Yu-Chun
Kuo, Po-Lin
LEAN-TEIK HUANG  
Kuo, Yueh-Hsiung
Lin, Chun-Ching
DOI
10.1016/j.canlet.2004.08.012
URI
https://www.scopus.com/pages/publications/15244358231?inward
Abstract
The fruiting body of Antrodia camphorata is well known in Taiwan as a traditional medicine for treating cancer and inflammation. The purpose of this study was to evaluate the apoptotic effects of ethylacetate extract from A. camphorata (EAC) fruiting bodies in two human liver cancer cell lines, Hep G2 and PLC/PRF/5. Treatment with EAC decreased the cell growth of Hep G2 and PLC/PRF/5 cells in a dose dependent manner. In Fas/APO-1 positive-Hep G2 cells, EAC increased the expression level of Fas/APO-1 and its two forms of ligands, membrane-bound Fas ligand (mFasL) and soluble Fas ligand (sFasL), in a p53-indenpendent manner. In addition, EAC also initiated mitochondrial apoptotic pathway through regulation of Bcl-2 family proteins expression, release of cytochrome c, and activation of caspase-9 both in Hep G2 and PLC/PRF/5 cells. Furthermore, EAC also inhibited the cell survival signaling by enhancing the amount of IκBα in cytoplasm and reducing the level and activity of NF-κB in the nucleus, and subsequently attenuated the expression of Bcl-XL in Hep G2 and PLC/PRF/5 cells. EAC therefore decreased the cell growth and induced apoptosis both in Hep G2 and PLC/PRF/5 cells.
Subjects
Antrodia camphorata
Apoptosis
Caspase
Fas ligand
Fas/APO-1
NF-κB
SDGs

[SDGs]SDG3

Other Subjects
acetic acid ethyl ester; antineoplastic agent; Antrodia camphorata extract; caspase 9; cytochrome c; Fas antigen; Fas ligand; immunoglobulin enhancer binding protein; protein bcl 2; protein bcl xl; protein p53; unclassified drug; antineoplastic activity; apoptosis; article; cancer cell culture; cancer growth; cell strain HepG2; cell survival; Chinese medicine; controlled study; cytoplasm; dose response; drug effect; enzyme activation; enzyme release; fruiting body; human; human cell; liver cell carcinoma; priority journal; protein expression; protein family
Publisher
Elsevier Ireland Ltd
Type
journal article

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