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

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...

Full description

Saved in:
Bibliographic Details
Published in:Cancer letters 2005-04, Vol.221 (1), p.77-89
Main Authors: Hsu, Ya-Ling, Kuo, Yu-Chun, Kuo, Po-Lin, Ng, Lean-Teik, Kuo, Yueh-Hsiung, Lin, Chun-Ching
Format: Article
Language:English
Subjects:
Antineoplastic Agents, Phytogenic
Antrodia camphorata
Apoptosis
Apoptosis - drug effects
Basidiomycota - chemistry
Cancer therapies
Carcinoma, Hepatocellular - pathology
Caspase
Cell culture
Cell cycle
Cell growth
Cell Proliferation - drug effects
Cytoplasm
Deoxyribonucleic acid
DNA
Drugs, Chinese Herbal - pharmacology
Enzymes
Fas ligand
Fas/APO-1
Hepatitis
Humans
Ligands
Liver cancer
Liver Neoplasms - pathology
NF-κB
Plant Extracts - pharmacology
Signal transduction
Signal Transduction - drug effects
Studies
Tumor Cells, Cultured
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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-X L 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.
ISSN:0304-3835
1872-7980
DOI:10.1016/j.canlet.2004.08.012