Expression of p53 and its mechanism in prostate cancer.

Abstract

The present study aimed to investigate the expression of tumor protein p53 (p53), and its mechanism of function, in prostate cancer (PC). Small interfering RNA (siRNA) was used to interfere with p53 expression in the PC cell line, DU145. Cell viability and p53 expression were analyzed using cell counting kit-8 (CCK-8) and western blotting. The effects of p53 expression on the proliferation, migration and adhesion abilities of PC cells were analyzed using Cell Counting kit-8, Transwell and adhesion assays. Changes in cell proliferation, migration and adhesion ability were observed following treatment with extracellular signal-regulated kinase (ERK) inhibitor, PD184352, and janus kinase (JNK) inhibitor, SP60012. The expression level of p53 declined 24 h after siRNA transfection (P<0.05). Furthermore, JNK and ERK, downstream proteins of the focal adhesion kinase (FAK)-Src proto-oncogene, non-receptor tyrosine kinase (Src) signaling pathway, were activated. These effects were associated with reduced proliferation, migration and adhesion abilities of PC cells compared with untransfected control cells (P<0.05). PD184352 and SP600125 treatments also resulted in reduced proliferation, migration and adhesion abilities of PC cells (P<0.05). In conclusion, PC cells exhibited low p53 expression, and the proliferation, migration and adhesion abilities of PC cells were promoted by inhibiting the activation of JNK and ERK. Together, these results suggest that p53 has potential as a therapeutic target in PC.