Cell experiments have found Pim‐2 may take part in the tumorigenesis of prostatic carcinoma (PCA). More direct evidences are needed, and the detailed anti‐apoptotic mechanism of Pim‐2 in PCA cells is still unknown.

Pim‐2 expression levels were compared between benign prostatic hyperplasia (BPH) tissues and PCA tissues using real time PCR and Western blot, respectively. Then Pim‐2 expression levels were detected in PCA cell lines DU‐145 and LNCaP, as well as in nontumorous prostatic epithelial cell lines RWPE‐1 and PNT1a, using real time PCR and Western blot, respectively. The co‐expression of Pim‐2 and eukaryotic initiation factor 4B (eIF4B) was examined by immunofluorescence cytochemistry using laser scanning confocal microscope. Finally, Pim‐2 SiRNA was transfected into DU‐145 cells and Pim‐2 was transfected into RWPE‐1 cells, and the level of Pim‐2 and phosphorylated eukaryotic initiation factor 4B (p‐eIF4B) were detected, as well as the apoptosis rate.

The Pim‐2 mRNA and protein level were significantly higher in PCA tissues than those in BPH tissues. The Pim‐2 mRNA and protein level in DU‐145 and LNCaP cells were significantly higher than those in RWPE‐1 and PNT1a cells. Pim‐2 and eIF4B could co‐express in DU‐145 cells. Pim‐2 level determined the phosphorylation level of eIF4B and the apoptosis rate of prostatic cells. The higher Pim‐2 expressed, the more eIF4B phosphorylated, then the less cell got apoptosis, and vice versa.

Pim‐2 was over‐expressed in PCA cell lines and tissues. It may inhibit the apoptosis of PCA cells through phosphorylating eIF4B, thus promote the tumorigenesis of PCA. Prostate 73: 1462–1469, 2013. © 2013 Wiley Periodicals, Inc.