Volume 1171, Issue 1 p. 495-500

Genistein Inhibits Cell Growth by Modulating Various Mitogen-Activated Protein Kinases and AKT in Cervical Cancer Cells

Su-Hyeon Kim

Su-Hyeon Kim

Cancer Research Institute, Seoul National University College of Medicine

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Su-Hyeong Kim

Su-Hyeong Kim

Cancer Research Institute, Seoul National University College of Medicine

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Yong-Beom Kim

Yong-Beom Kim

Cancer Research Institute, Seoul National University College of Medicine

Department of Obstetrics and Gynecology

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Yong-Tark Jeon

Yong-Tark Jeon

Cancer Research Institute, Seoul National University College of Medicine

Department of Obstetrics and Gynecology

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Sang-Chul Lee

Sang-Chul Lee

Institute of Complementary and Integrative Medicine, Medical Research Center, College of Medicine

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Yong-Sang Song

Yong-Sang Song

Department of Obstetrics and Gynecology

Institute of Complementary and Integrative Medicine, Medical Research Center, College of Medicine

Major in Biomodulation, World Class University, Seoul National University, Seoul, Korea

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First published: 15 August 2009
Citations: 52
Address for correspondence: Yong-Sang Song, M.D., Ph.D., Department of Obstetrics and Gynecology, Seoul National University College of Medicine, 28 Yongun-dong, Chongno-gu, Seoul, 110-744, Korea. Voice: 82-2-2072-2822; fax: 82-2-3668-7401. [email protected]

Abstract

Genistein, a soy-derived isoflavone, inhibits growth of tumor cells from various malignancies. Here we investigated the effect of genistein on the growth of cervical cancer cells (HeLa and CaSki) and its possible mechanism. Genistein significantly suppressed cell growth of HeLa and CaSki cells at concentrations of 20 and 60 μmol/L, respectively, for 24 h. Western blotting analysis showed that genistein reduced phosphorylation of AKT and extracellular signal–regulated kinase (ERK)-1/2 and induced phosphorylation of p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK). Moreover, inhibition of ERK1/2 activity enhanced cell growth inhibition by genistein, whereas inhibition of p38 MAPK activity rescued from genistein-mediated growth inhibition. Interestingly, inhibition of AKT activity recovered genistein-induced growth inhibition in CaSki cells but did not in HeLa cells. However, inhibition of JNK activity seemed to have little effect on cell growth inhibition by genistein. Taken together, these results suggest that genistein could inhibit cell growth by inhibiting ERK1/2 activity and activating p38 MAPK.