Expression of phosphatidylinositol 3 kinase/protein kinase B signaling pathway in bladder cancer cells and its relationship with cancer stem cells

Abstract

Objective To examine the expression of phosphatidylinositol 3 kinase (PI3K)/protein kinase B (Akt) signaling pathway in bladder cancer cells, and demonstrate relationship with cancer stem cells. Methods The expression of PI3K, phosphorylated protein kinase B (p-Akt) in bladder cancer cells was detected by reverse transcription-polymeric chain reaction (RT-PCR) and Western blotting. Double immunofluorescence analysis was applied to detect the expression of CD133, the Co-expression of p-Akt and CD133. CD133 is one of surface marker of bladder cancer stem cells. Results We detected a strong up-regulation of PI3K, p-Akt (PI3K protein: 1.05±0.03, p-Akt protein: 1.21±0.04, PI3K mRNA: 0.68±0.03) in bladder cancer tissue samples compared to normal bladder tissues (PI3K protein: 0.68±0.04, p-Akt protein: 0.71±0.02, PI3K mRNA: 0.42±0.02) by Western blot and RT-PCR approaches. We also detected a strong Co-expression of p-Akt and CD133 in bladder cancer tissue samples. Conclusion The expression of PI3K/Akt signaling pathway is up-regulation in bladder cancer tissues, and the expression of CD133 and p-Akt was co-expressed, suggesting that the activation and differentiation of bladder cancer stem cells could be inhibited by interference with PI3K/Akt signaling pathway to prevent the occurrence and development of bladder cancer. Key words: Bladder cancer; Bladder cancer stem cell; Phosphatidylinositol 3 kinase/protein kinase B signaling pathway