Individual and interactive effects of apigenin analogs on G2/M cell-cycle arrest in human colon carcinoma cell lines

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. Cellul...

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Published in:Nutrition and cancer 2004, Vol.48 (1), p.106-114
Main Authors: Wang, W, VanAlstyne, P.C, Irons, K.A, Chen, S, Stewart, J.W, Birt, D.F
Format: Article
Language:English
Subjects:
acacetin
anticarcinogenic activity
Antineoplastic Agents - pharmacology
apigenin
Apigenin - chemistry
Apigenin - pharmacology
Biological and medical sciences
Caco-2 Cells
cell cycle
Cell Division - drug effects
cell growth
cell lines
Cell Survival - drug effects
Chromatography, High Pressure Liquid
chrysin
Colonic Neoplasms
colorectal neoplasms
Dose-Response Relationship, Drug
Feeding. Feeding behavior
flavones
Flow Cytometry
Fundamental and applied biological sciences. Psychology
G2 Phase - drug effects
human health
Humans
interphase
kampherol
luteolin
Medical sciences
Metabolic diseases
mitosis
Mitosis - drug effects
myricetin
naringenin
phytochemicals
quercetin
Tumor Cells, Cultured
Tumors
Vertebrates: anatomy and physiology, studies on body, several organs or systems
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Summary: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 micromolar 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 micromolar, but the percentage of cells in G2/M decreased at doses greater than 40 micromolar. 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 micromolar with apigenin at 20 micromolar, 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 micromolar were combined with apigenin at 20 micromolar, there was an increase of 22% in the proportion of G2/M cells over that observed with 20 micromolar apigenin alone (P < 0.05). At doses higher than 40 micromolar, 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 micromolar 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 conjo
ISSN:0163-5581
1532-7914
DOI:10.1207/s15327914nc4801_14