Objective  To explore whether protein kinase D3 (PKD3) has an effect on Etoposide - induced growth inhibition in hormonal refractory prostate cancer (HPRC) cells. Methods The human prostate cancer DU - 145 cells were transfected with siRNA of non - specific control (si - CTL)

and siRNA of PKD3 (si - PKD3 - 1

si - PKD3 - 2) respectively. The expre

ssion of PKD3 in the transfected cells was measured by Western blot analysis. The DU - 145 cells transfected with siRNA after 48 h were treated with 0

30

70

100

or 300 μ mol/L of Etoposide for 24 h. In addition

the DU - 145 cells were also treated with PKC inhibitor (Go6983

5 μ mol/L)

PKC - PKD inhibitor (Go6976

5 μ mol/L)

or the 2 agents combined with Etoposide respectively for 24 h

cell lysates were harvested and measured by CellTiter - Glo

?

Luminescent Cell Viability Assay kit. Results Silence of endogenous PKD3 was confirmed in the DU - 145 transfected with si - RNA - PKD3 by Western blot analysis. Cell viability assay showed that cell growth in DU - 145 cells transfected with si - CTL was inhibited in a dose - dependent manner after treatment of Etoposide. Furthermore

silence of endogenous PKD3 expression not only significantly inhibited DU - 145 cell growth (

P

0.01)

but also dramatically enhanced cell growth inhibition response to Etoposide (

P

0.01). Moreover

the DU - 145 cell growth was also inhibited by PKC - PKD double inhibitor Go6976

whereas slightly inhibited by single PKC inhibitor Go6983. Conclusion Reduced PKD3 expression and activity can enhance cell growth inhibitory and sensitivity to Etoposide in HPRC cells

suggesting that PKD3 may be as a potential therapeutic target in human prostate cancer therapy.