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Title 

Ginkgetin inhibits the growth of DU­145 prostate cancer cells through inhibition of signal transducer and activator of transcription 3 activity

 

Ginkgetin의 항암 효과

Authors 

Yoon Jung JeonSeung Nam JungJieun YunChang Woo LeeJiyoun ChoiYu Jin LeeDong Cho HanByoung-Mog Kwon

Publisher 

Wiley-Blackwell

Issue Date 

2015

Citation 

Cancer Science, vol. 106, no. 4, pp. 413-420

Keywords 

ApoptosisBiflavonoidGinkgetinProstate cancerSTAT3

Abstract 

Signal transducer and activator of transcription 3 (STAT3) is constitutively activated in human cancers. Therefore, STAT3 is a therapeutic target of cancer drug discovery. We previously reported that natural products inhibited constitutively activated STAT3 in human prostate tumor cells. We used a dual-luciferase assay to screen 200 natural products isolated from herbal medicines and we identified ginkgetin obtained from the leaves of Ginkgo biloba L. as a STAT3 inhibitor. Ginkgetin inhibited both inducible and constitutively activated STAT3 and blocked the nuclear translocation of p-STAT3 in DU-145 prostate cancer cells. Furthermore, ginkgetin selectively inhibited the growth of prostate tumor cells stimulated with activated STAT3. Ginkgetin induced STAT3 dephosphorylation at Try705 and inhibited its localization to the nucleus, leading to the inhibition of expression of STAT3 target genes such as cell survival-related genes (cyclin D1 and survivin) and anti-apoptotic proteins (Bcl-2 and Bcl-xL). Therefore, ginkgetin inhibited the growth of STAT3-activated tumor cells. We also found that ginkgetin inhibited tumor growth in xenografted nude mice and downregulated p-STAT3Tyr705 and survivin in tumor tissues. This is the first report that ginkgetin exerts antitumor activity by inhibiting STAT3. Therefore, ginkgetin is a good STAT3 inhibitor and may be a useful lead molecule for development of a therapeutic STAT3 inhibitor.

ISSN 

1347-9032

Link 

http://dx.doi.org/10.1111/cas.12608

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2017-04-19


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