Abstract
The effect of some flavonoids, which are components of fruits, vegetables, and peas, on the cell cycle progression of human LNCaP prostate cancer cells has been investigated in this study. Genistein arrested the cell cycle at the G2/M phases, which is attributed to the suppression of cyclin B expression. In addition, genistein induced the cyclin-dependent kinase inhibitor p21, which does not depend on p53 activation. Apigenin and luteolin also increased p21 levels, but quercetin did not. Apigenin induced p21 production through a p53-dependent pathway, but luteolin did so in a p53-independent manner. These results suggest that flavonoids are potent regulators of cyclin B and p21 for cell cycle progression, which may play some roles in prevention of carcinogenesis.
MeSH terms
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Animals
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Antineoplastic Agents / pharmacology
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Apigenin
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Cell Cycle / drug effects*
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Cyclin B / biosynthesis
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Dose-Response Relationship, Drug
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Expectorants / pharmacology
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Flavonoids / pharmacology*
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Flow Cytometry
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G2 Phase
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Genes, p53 / genetics
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Genistein / pharmacology
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Humans
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Immunoblotting
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Luteolin
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Male
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Mice
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Mice, Inbred BALB C
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Mitosis
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Models, Chemical
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Phosphorylation
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Precipitin Tests
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Prostatic Neoplasms / drug therapy
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Prostatic Neoplasms / metabolism*
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Proto-Oncogene Proteins p21(ras) / biosynthesis
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Quercetin / pharmacology
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Tumor Cells, Cultured
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Tumor Suppressor Protein p53 / metabolism
Substances
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Antineoplastic Agents
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Cyclin B
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Expectorants
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Flavonoids
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Tumor Suppressor Protein p53
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Apigenin
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Quercetin
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Genistein
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HRAS protein, human
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Proto-Oncogene Proteins p21(ras)
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Luteolin