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Carcinogenesis Advance Access published online on October 25, 2006
Carcinogenesis, doi:10.1093/carcin/bgl189
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© The Author 2006. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org
Received March 29, 2006
Revised September 27, 2006
Accepted September 29, 2006

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION

Luteolin inhibits insulin-like growth factor 1 receptor signaling in prostate cancer cells

Jing Fang 1 * *, Qiong Zhou 1 *, Xiang-lin Shi 1, and Bing-hua Jiang 2

1 The Institute for Nutritional Sciences, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences, Graduate School of Chinese Academy of Sciences, Shanghai 200031, China
2 The Institute for Nutritional Sciences, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences, Graduate School of Chinese Academy of Sciences, Shanghai 200031, China; The Department of Microbiology, Cell Biology and Immunology, MBR Cancer Center, West Virginia University, Morgantown, WV 26506, USA

* To whom correspondence should be addressed.
Jing Fang, E-mail: jfang{at}sibs.ac.cn


  Abstract

Insulin-like growth factor receptor (IGF-1R) activation is required for prostate cell proliferation. Prostate cancer is one of the most commonly diagnosed malignant tumors in Western countries. Overexpression of IGF-1R in prostate cancer is associated with tumor growth. These suggest that IGF-1R-inhibitory agents may be of preventive and/or therapeutic value. With evidence accumulating for a chemopreventive role of flavonoids, the effects of luteolin, a bioactive flavonoid, on IGF-1R signaling in prostate cancer cells were examined. Luteolin inhibited insulin-like growth factor 1 (IGF-1)-induced activation of IGF-1R and AKT in prostate cancer PC-3 and DU145 cells. Inhibition of AKT by luteolin resulted in decreased phosphorylation of its downstream targets, including p70S6K1, GSK-3{beta}, and FKHR/FKHRL1. Luteolin also inhibited the IGF-1-induced activation of EGFR and MAPK/ERK signaling. Luteolin inhibited expression of cyclin D1 and increased expression of p21. As a result, luteolin suppressed proliferation and induced apoptosis of prostate cancer cells. Knockdown of IGF-1R by siRNA led to inhibition of proliferation of prostate cancer cells. Results of in vivo tumor growth assay indicated that luteolin inhibited PC-3 tumor growth. Immunoblotting of the extracts of tumor tissues showed that luteolin inhibited IGF-1R/AKT signaling. Our results provide a new insight into the mechanisms that luteolin is against cancer cells.

*These two people contributed equally to this work.
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