Author/Authors :
Seward، نويسنده , , Shelly and Semaan، نويسنده , , Assaad and Qazi، نويسنده , , Aamer M. and Gruzdyn، نويسنده , , Oksana V. and Chamala، نويسنده , , Sreedhar and Bryant، نويسنده , , Christopher C. and Kumar، نويسنده , , Sanjeev and Cameron، نويسنده , , David and Sethi، نويسنده , , Seema and Ali-Fehmi، نويسنده , , Rouba and Morris، نويسنده , , Robert and Bouwman، نويسنده , , David L. and Munkarah، نويسنده , , Adnan R. and Weaver، نويسنده , , Donald W. and Gruber، نويسنده , , Scott A. and Batchu، نويسنده , , Ramesh B.، نويسنده ,
Abstract :
The enhancer of zeste homolog 2 (EZH2) methyltransferase is a transcriptional repressor. EZH2 is abnormally elevated in epithelial ovarian cancer (EOC). We demonstrated that EZH2 knockdown inhibited cell growth, activated apoptosis, and enhanced chemosensitivity. Further, silencing of EZH2 resulted in re-expression of p21waf1/cip1 and down-regulation of mutant p53. Finally, EZH2 knockdown contributed to attenuated EOC growth in SCID mice.
Keywords :
m p53 , Enhancer of zeste homolog 2 (EZH2) , RNA interference (RNAi) , Epithelial ovarian cancer (EOC) , p21Waf1/Cip1
