期刊
CANCER LETTERS
卷 313, 期 1, 页码 84-90出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2011.08.026
关键词
Prostate cancer; Everolimus resistance; Tumor growth; Cdk1; Cyclin B
类别
资金
- Jung-Stiftung
- Alfons und Getrud Kassel-Stiftung
The growth potential of PC3 prostate cancer cells, sensible (PC3(par)) or resistant (PC3(res)) to the mTOR inhibitor everolimus (RAD001) was investigated. Cell growth and proliferation of PC3(res) was similar to that of PC3(par), and late apoptosis increased in PC3(par) but decreased in PC3(res) following treatment with low dosed everolimus. PC3(res) accumulated in the G2/M-phase, accompanied by cdk1, cdk2 and cyclin B elevation. Knocking down cdk1 or cyclin B distinctly blocked the growth activity of PC3(res). One reason for everolimus resistance may be up-regulation of the cdk1-cyclin B complex in prostate cancer cells, leading to enhanced progression towards G2/M. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
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