TY - JOUR
T1 - Induction of cell cycle arrest in prostate cancer cells by the dietary compound isoliquiritigenin
AU - Lee, Yeo Myeong
AU - Lim, Do Young
AU - Choi, Hyun Ju
AU - Jung, Jae In
AU - Chung, Won Yoon
AU - Park, Jung Han Yoon
PY - 2009/2/1
Y1 - 2009/2/1
N2 - Isoliquiritigenin (ISL), a flavonoid chalcone that is present in licorice, shallot, and bean sprouts, is known to have antitumorigenic activities. The present study examined whether ISL alters prostate cancer cell cycle progression. DU145 human and MatLyLu (MLL) rat prostate cancer cells were cultured with various concentrations of ISL. In both DU145 and MLL cells treated with ISL, the percentage of cells in the G1 phase increased, and the incorporation of [3H]thymidine decreased. ISL decreased the protein levels of cyclin D1, cyclin E, and cyclin-dependent kinase (CDK) 4, whereas cyclin A and CDK2 expressions were unaltered in cells treated with ISL. The expression of the CDK inhibitor p27KIP1 was increased in cells treated with 20 μmol/L ISL. In addition, treatment of cells with 20 μmol/L ISL for 24 hours led to G2/M cell cycle arrest. Cell division control (CDC) 2 protein levels remained unchanged. The protein levels of phospho-CDC2 (Tyr15) and cyclin B1 were increased, and the CDC25C level was decreased by ISL dose-dependently. We demonstrate that ISL promotes cell cycle arrest in DU145 and MLL cells, thereby providing insights into the mechanisms underlying its antitumorigenic activities.
AB - Isoliquiritigenin (ISL), a flavonoid chalcone that is present in licorice, shallot, and bean sprouts, is known to have antitumorigenic activities. The present study examined whether ISL alters prostate cancer cell cycle progression. DU145 human and MatLyLu (MLL) rat prostate cancer cells were cultured with various concentrations of ISL. In both DU145 and MLL cells treated with ISL, the percentage of cells in the G1 phase increased, and the incorporation of [3H]thymidine decreased. ISL decreased the protein levels of cyclin D1, cyclin E, and cyclin-dependent kinase (CDK) 4, whereas cyclin A and CDK2 expressions were unaltered in cells treated with ISL. The expression of the CDK inhibitor p27KIP1 was increased in cells treated with 20 μmol/L ISL. In addition, treatment of cells with 20 μmol/L ISL for 24 hours led to G2/M cell cycle arrest. Cell division control (CDC) 2 protein levels remained unchanged. The protein levels of phospho-CDC2 (Tyr15) and cyclin B1 were increased, and the CDC25C level was decreased by ISL dose-dependently. We demonstrate that ISL promotes cell cycle arrest in DU145 and MLL cells, thereby providing insights into the mechanisms underlying its antitumorigenic activities.
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U2 - 10.1089/jmf.2008.0039
DO - 10.1089/jmf.2008.0039
M3 - Article
C2 - 19298190
AN - SCOPUS:64949183401
SN - 1096-620X
VL - 12
SP - 8
EP - 14
JO - Journal of medicinal food
JF - Journal of medicinal food
IS - 1
ER -
