Author/Authors :
Tsaur، نويسنده , , Igor and Makarevi?، نويسنده , , Jasmina and Hudak، نويسنده , , Lukasz and Juengel، نويسنده , , Eva and Kurosch، نويسنده , , Martin and Wiesner، نويسنده , , Christoph and Bartsch، نويسنده , , Georg and Harder، نويسنده , , Sebastian and Haferkamp، نويسنده , , Axel and Blaheta، نويسنده , , Roman A.، نويسنده ,
Abstract :
The growth potential of PC3 prostate cancer cells, sensible (PC3par) or resistant (PC3res) to the mTOR inhibitor everolimus (RAD001) was investigated. Cell growth and proliferation of PC3res was similar to that of PC3par, and late apoptosis increased in PC3par but decreased in PC3res following treatment with low dosed everolimus. PC3res 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 PC3res. 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.
Keywords :
prostate cancer , Tumor growth , Everolimus resistance , cyclin B , CDK1
