Evodiamine, a constituent of Evodiae Fructus, induces anti‐proliferating effects in tumor cells

We found that evodiamine, a major alkaloidal component of Evodiae Fructus (Goshuyu in Japan), inhibited proliferation of several tumor cell lines, but had less effect on human peripheral blood mononuclear cells (PBMC). We used human cervical cancer cells, HeLa, as a model to elucidate the molecular...

Full description

Saved in:

Bibliographic Details
Published in:	Cancer science Vol. 94; no. 1; pp. 92 - 98
Main Authors:	Fei, Xiao Fang, Wang, Ben Xiang, Li, Tei Jin, Tashiro, Shin‐ichi, Minami, Mutsuhiko, Xing, De Jun, Ikejima, Takashi
Format:	Journal Article
Language:	English
Published:	Oxford, UK Blackwell Publishing Ltd 01-01-2003 Blackwell John Wiley & Sons, Inc
Subjects:	Alkaloids - chemistry Alkaloids - pharmacology Amino Acid Chloromethyl Ketones - pharmacology Animals Antineoplastic Agents, Phytogenic - pharmacology Apoptosis Apoptosis - drug effects BAX gene bcl-2-Associated X Protein Biological and medical sciences Caspase Caspase 3 Caspases - metabolism Cell death Cell Division - drug effects Cervical cancer Cervix Cysteine Proteinase Inhibitors - pharmacology Dactinomycin - pharmacology Deoxyribonucleic acid DNA DNA fragmentation DNA Fragmentation - drug effects Drug Screening Assays, Antitumor Enzyme Activation - drug effects Evodia - chemistry Fibrosarcoma - pathology Fluorouracil - pharmacology Furans - chemistry Furans - pharmacology Gene expression Gene Expression Regulation, Neoplastic - drug effects General pharmacology Genes, bcl-2 - drug effects HeLa Cells - drug effects HeLa Cells - enzymology Hepatocytes - drug effects Heterocyclic Compounds, 4 or More Rings - chemistry Heterocyclic Compounds, 4 or More Rings - pharmacology Humans Indole Alkaloids Leukemia, Monocytic, Acute - pathology Leukocytes (mononuclear) Leukocytes, Mononuclear - drug effects Medical sciences Melanoma - pathology Mice Mitochondria Mitochondria - drug effects Molecular modelling Molecular Structure Neoplasm Proteins - metabolism Oligopeptides - pharmacology Peripheral blood mononuclear cells Pharmacognosy. Homeopathy. Health food Pharmacology. Drug treatments Plant Extracts - chemistry Plant Extracts - pharmacology Proto-Oncogene Proteins - biosynthesis Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins c-bcl-2 - biosynthesis Quinazolines - chemistry Quinazolines - pharmacology Rats Rats, Inbred BUF Sarcoma 180 - pathology Tumor cell lines Tumor cells Tumor Cells, Cultured - drug effects Tumor Cells, Cultured - enzymology Antineoplastic agent Carcinoma Cysteine endopeptidases Rutaceae Homology Uterine cervix Fragmentation Chinese medicine Folk medicine Dicotyledones Angiospermae Established cell line Caspase 3 Genetics Mechanism of action Protooncogene Human Enzyme Pharmacognosy Malignant tumor In vitro Hela cell line Biological activity Peptidases Cell death DNA C-Onc gene Alternative medicine Plant origin Hydrolases Spermatophyta Apoptosis
Online Access:	Get full text
Tags:	Add Tag No Tags, Be the first to tag this record!

Description
Summary:	We found that evodiamine, a major alkaloidal component of Evodiae Fructus (Goshuyu in Japan), inhibited proliferation of several tumor cell lines, but had less effect on human peripheral blood mononuclear cells (PBMC). We used human cervical cancer cells, HeLa, as a model to elucidate the molecular mechanisms of evodiamine‐induced tumor cell death. The results showed that evodiamine induced oligonucleosomal fragmentation of DNA in HeLa cells and increased the activity of caspase‐3, but not that of caspase‐1, in vitro. Both evodiamine‐induced DNA fragmentation and caspase‐3 activity were effectively inhibited by a caspase‐3 inhibitor, z‐DEVD‐fmk (z‐Asp‐Glu‐Val‐Asp‐fmk). In addition, evodiamine increased the expression of the apoptosis inducer Bax, but decreased the expression of the apoptosis suppressor Bcl‐2 in mitochondria. Taken together, our data indicated that evodiamine alters the balance of Bcl‐2 and Bax gene expression and induces apoptosis through the caspase pathway in HeLa cells. (Cancer Sci 2003; 94: 92–98)
Bibliography:	To whom correspondence should be addressed. E‐mail ikejimat@vip.sina.com ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 To whom correspondence should be addressed. E‐mail: ikejimat@vip.sina.com
ISSN:	1347-9032 1349-7006
DOI:	10.1111/j.1349-7006.2003.tb01358.x