Document Detail


Impact of adenomatous polyposis coli (APC) tumor supressor gene in human colon cancer cell lines on cell cycle arrest by apigenin.
MedLine Citation:
PMID:  17620292     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
This research assessed the importance of the adenomatous polyposis coli (APC) tumor suppressor mutation in the ability of apigenin to induce cell cycle arrest using HT29-APC cells, which contain inducible wild-type APC under the metallothionein promoter. HT29-GAL cells, containing beta-galactosidase (GAL), were included as control. Treatment with apigenin (0, 20, 40, 60, and 80 microM) for 48 h resulted in reduction in the cell number (P < 0.05) concurrent with flow cytometry results showing a dose-dependent accumulation of cells in the G2/M phase in both HT29-APC and HT29-GAL cells without ZnCl(2) treatment. Flow cytometric analysis showed an increase (P < 0.05) in the percentage of cells in G2/M when HT29-APC cells were treated with 80 microM apigenin for 120 h. This increase was not present in HT29-APC cells when treated with both 80 microM apigenin and 100 microM ZnCl(2) for 120 h. Western blot analysis verified the induction of APC protein expression in ZnCl(2)-treated HT29-APC cells but not in ZnCl(2)-treated HT29-GAL cells. Apigenin plus ZnCl(2) treatment increased the expression of APC protein in HT29-APC cells by 50 fold above expression observed with ZnCl(2) alone. Upon induction of the APC gene with ZnCl(2) in HT29-APC cells, the percentage of apoptotic cells increased significantly (P < 0.05) after 120-h treatment. Additionally, apigenin treatment (80 microM) further increased the percentage of apopototic HT29-APC following ZnCl(2) treatment to induce wild-type APC expression. These results suggest that APC dysfunction may be critical for apigenin to induce cell cycle arrest in human colon cancer cell lines and furthermore, apigenin enhances APC expression and apoptosis in cells with wild-type APC.
Authors:
C S Chung; Y Jiang; D Cheng; D F Birt
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Molecular carcinogenesis     Volume:  46     ISSN:  0899-1987     ISO Abbreviation:  Mol. Carcinog.     Publication Date:  2007 Sep 
Date Detail:
Created Date:  2007-08-27     Completed Date:  2007-11-13     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8811105     Medline TA:  Mol Carcinog     Country:  United States    
Other Details:
Languages:  eng     Pagination:  773-82     Citation Subset:  IM    
Copyright Information:
(c) 2007 Wiley-Liss, Inc.
Affiliation:
Department of Food Science and Human Nutrition, Iowa State University, Ames, Iowa 50011, USA.
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MeSH Terms
Descriptor/Qualifier:
Adenomatous Polyposis Coli Protein / genetics*,  metabolism
Apigenin / pharmacology*
Apoptosis / drug effects
Cell Count
Cell Cycle / drug effects*
Cell Proliferation / drug effects
Chlorides / pharmacology
Colonic Neoplasms / metabolism*,  pathology*
Dose-Response Relationship, Drug
Drug Interactions
Flow Cytometry
G2 Phase / drug effects
HT29 Cells
Humans
Mitosis / drug effects
Time Factors
Tumor Cells, Cultured
Zinc Compounds / pharmacology
Chemical
Reg. No./Substance:
0/Adenomatous Polyposis Coli Protein; 0/Chlorides; 0/Zinc Compounds; 520-36-5/Apigenin; 7646-85-7/zinc chloride

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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