Document Detail

Individual and interactive effects of apigenin analogs on G2/M cell-cycle arrest in human colon carcinoma cell lines.
MedLine Citation:
PMID:  15203384     Owner:  NLM     Status:  MEDLINE    
Apigenin has been previously shown to induce G2/M cell-cycle arrest in human colon cancer cell lines. The present study assessed the individual and interactive influence of seven apigenin analogs on cell cycle, cell number, and cell viability in human SW480 and Caco-2 colonic carcinoma cells. Cellular concentration of selected apigenin analogs was further assessed by high-performance liquid chromatography to assess cellular availability. The apigenin analogs studied were acacetin, chrysin, kampherol, luteolin, myricetin, naringenin, and quercetin. DNA flow cytometric analysis indicated that treatment with either chrysin or acacetin at 0 to 80 microM for 48 h resulted in cell-cycle arrest at the G2/M phase in a dose-dependent manner in the SW480 cells but not in the Caco-2 cells. The percentage of SW480 cells at G2/M also increased when cells were treated with kampherol, luteolin, or quercetin between 5 and 30 microM, but the percentage of cells in G2/M decreased at doses greater than 40 microM. Cell number was significantly decreased in a time- and dose-dependent manner following the treatments with each analog except for naringenin and myricetin. The interactive effects of these analogs with apigenin were further assessed by combining each analog at doses from 0 to 80 microM with apigenin at 20 microM, a dose at which apigenin was found to double the proportion of SW480 cells in G2/M. When either acacetin, chrysin, luteolin, kampherol, or quercetin at doses between 5 and 30 microM were combined with apigenin at 20 microM, there was an increase of 22% in the proportion of G2/M cells over that observed with 20 microM apigenin alone (P < 0.05). At doses higher than 40 microM, however, the interaction became antagonistic, and the proportion of cells in G2/M decreased below that observed with apigenin alone. Cell viability, as assessed by Trypan blue exclusion assay, significantly decreased by treatments with high doses of each agent or each agent combined with apigenin. Cellular concentration of apigenin, chrysin, or naringenin in SW480 cells significantly increased at doses of 40 microM or greater, but it was not correlated with their impact on G2/M cell-cycle arrest. The induction of cell-cycle arrest by five of seven tested apigenin analogs and the additive induction by the combination of flavonoids at low doses suggest that apigenin-related flavonoids may cooperatively protect against colorectal cancer through conjoint blocking of cell-cycle progression.
Weiqun Wang; Peter C VanAlstyne; Kimberly A Irons; She Chen; Jeanne W Stewart; Diane F Birt
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.    
Journal Detail:
Title:  Nutrition and cancer     Volume:  48     ISSN:  0163-5581     ISO Abbreviation:  Nutr Cancer     Publication Date:  2004  
Date Detail:
Created Date:  2004-06-18     Completed Date:  2004-12-02     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  7905040     Medline TA:  Nutr Cancer     Country:  United States    
Other Details:
Languages:  eng     Pagination:  106-14     Citation Subset:  IM    
Copyright Information:
Copyright 2004 Lawrence Erlbaum Associates, Inc.
Department of Food Science and Human Nutrition, Iowa State University, Ames 50011, USA.
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MeSH Terms
Antineoplastic Agents / pharmacology*
Apigenin / chemistry*,  pharmacology*
Caco-2 Cells
Cell Division / drug effects
Cell Survival / drug effects
Chromatography, High Pressure Liquid
Colonic Neoplasms
Dose-Response Relationship, Drug
Flow Cytometry
G2 Phase / drug effects*
Mitosis / drug effects*
Tumor Cells, Cultured
Reg. No./Substance:
0/Antineoplastic Agents; 520-36-5/Apigenin

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

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