The over-expression of Pim-2 promote the tumorigenesis of prostatic carcinoma through phosphorylating eIF4B.

BACKGROUND: 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.
METHODS: 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.
RESULTS: 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.
CONCLUSION: 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.