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Pim-2 Cooperates with Downstream Factor XIAP to Inhibit Apoptosis and Intensify Malignant Grade in Prostate Cancer
Ke Ren1, Xin Gou2, Mingzhao Xiao2
1Department of Urology, The First Affiliated Hospital of Chongqing Medical University, 1 Youyi Road, Yuzhong Distrct, Chongqing, 400016, People's Republic of China. renke_rk@163.com.
Abstract:
To find the exact downstream effector of Pim-2 pathway in prostate cancer cells, and to determine the means by which it affects prostate cancer. XIAP, Pim-2 and p-eIF4B expressions were detected in PCA and BPH tissues. Then the Pim-2 and XIAP expressions were manipulated using transfection or RNAi in prostatic cells. Finally, Pim-2/eIF4B/XIAP levels were examined in PCA tissues with different clinicopathologic features. XIAP was significantly higher in PCA than in BPH tissues. When Pim-2 was transfected into noncancerous prostate epithelial cells RWPE-1, Pim-2, p-eIF4B and XIAP were all significantly increased and the apoptosis rate was significantly decreased. When XIAP was transfected into RWPE-1 cells, XIAP was significantly increased with no impact on Pim-2, p-eIF4B and the apoptosis rate. When Pim-2 SiRNA was transfected into prostate cancer cells PC-3, Pim-2, p-eIF4B and XIAP were significantly decreased and the apoptosis rate was significantly increased. When XIAP SiRNA was transfected into PC-3 cells, XIAP was significantly decreased with no impact on Pim-2, p-eIF4B and apoptosis rate. Pim-2, p-eIF4B and XIAP were all significantly higher in PCA tissues with GS ≥8 than those with GS ≤7. XIAP is the downstream factor of Pim-2 pathway in prostate cancer cells. Pim-2 and XIAP cooperate in inhibiting the apoptosis of prostate cancer cells. The activation of Pim-2 pathway may predict higher GS in prostate cancer.
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