Document Detail

Enterolactone induces apoptosis and inhibits growth of Colo 201 human colon cancer cells both in vitro and in vivo.
MedLine Citation:
PMID:  16158974     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: The mammalian lignan enterolactone (ENL) is produced from plant lignans which are present in large amounts in flaxseed (linseed). The effect of ENL on colon cancer cell growth in vitro and in vivo, and its mechanisms of action, have not been studied in detail. MATERIALS AND METHODS: The growth of the colo 201 human colon cancer cell line was examined by colorimetric 3-(4,5-dimethylthiazol-2-yl)-5- (3-carboxymethoxyphenyl)-2- (4-sulphophenyl)-2H-tetrazolium (MTS) assay, while the expression of apoptosis- and proliferation-related proteins (p53, Bax, Bcl-xL and S, Bcl-2, Caspase-8, Caspase-3 and proliferating cell nuclear antigen (PCNA)) were examined by Western blotting. In vivo tumor growth was examined by transplanting colo 201 cells into ENL-treated and placebo-treated athymic mice. RESULTS: The MTS assay showed that ENL suppressed colo 201 cell growth (IC50 for 72 h: 118.4 microM) in vitro. On flow cytometry, induction of apoptosis was confirmed by the appearance of subG1 populations, while cell cycle progression was not affected. The expression of an apoptosis-suppressing protein (Bcl-2) was down-regulated, an apoptosis-enhancing protein (cleaved form of Caspase-3) was up-regulated, proliferation-related PCNA protein was down-regulated and p53, Bax, Bcl-xL and S and Caspase-8 levels were unchanged. ENL, at a dose of 10 mg/kg given 3 times per week by subcutaneous injection, significantly inhibited the growth of colo 201 cells transplanted into athymic mice without any adverse effects. CONCLUSION: ENL suppressed colo 201 human colon cancer cell growth both in vitro and in vivo. The tumor-suppressing mechanisms included apoptosis and decreased cell proliferation.
Naoyuki Danbara; Takashi Yuri; Miki Tsujita-Kyutoku; Reiko Tsukamoto; Norihisa Uehara; Airo Tsubura
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Anticancer research     Volume:  25     ISSN:  0250-7005     ISO Abbreviation:  Anticancer Res.     Publication Date:    2005 May-Jun
Date Detail:
Created Date:  2005-09-14     Completed Date:  2005-11-02     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8102988     Medline TA:  Anticancer Res     Country:  Greece    
Other Details:
Languages:  eng     Pagination:  2269-76     Citation Subset:  IM    
Department of Pathology II, Kansai Medical University, Moriguchi, Osaka 570-8506, Japan.
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MeSH Terms
4-Butyrolactone / analogs & derivatives*,  pharmacology
Adenocarcinoma / drug therapy*,  pathology
Apoptosis / drug effects*
Caspase 3
Caspase 8
Caspases / metabolism
Cell Growth Processes / drug effects
Cell Line, Tumor
Colonic Neoplasms / drug therapy*,  pathology
Cyclin D1 / metabolism
Flow Cytometry
Lignans / pharmacology*
Mice, Nude
Proliferating Cell Nuclear Antigen / metabolism
Proto-Oncogene Proteins c-bcl-2 / metabolism
Tumor Suppressor Protein p53 / metabolism
bcl-2-Associated X Protein
bcl-X Protein
Reg. No./Substance:
0/BAX protein, human; 0/BCL2L1 protein, human; 0/Bax protein, mouse; 0/Bcl2l1 protein, mouse; 0/Lignans; 0/Proliferating Cell Nuclear Antigen; 0/Proto-Oncogene Proteins c-bcl-2; 0/Tumor Suppressor Protein p53; 0/bcl-2-Associated X Protein; 0/bcl-X Protein; 136601-57-5/Cyclin D1; 76543-15-2/2,3-bis(3'-hydroxybenzyl)butyrolactone; 96-48-0/4-Butyrolactone; EC 3.4.22.-/CASP3 protein, human; EC 3.4.22.-/CASP8 protein, human; EC 3.4.22.-/Casp3 protein, mouse; EC 3.4.22.-/Casp8 protein, mouse; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspase 8; EC 3.4.22.-/Caspases

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