Platelet-activating factor receptor activation promotes prostate cancer cell growth, invasion and metastasis via ERK1/2 pathway.

Abstract

Platelet-activating factor (PAF) and its receptor (PAFR), have been reported to participate in many cellular processes of cancer. However, little is known about their function in prostate cancer. In the present study, we found that PAFR was overexpressed in prostate cancer cells. PAF stimulation dose-dependently promoted the invasion, migration and growth of prostate cancer cells invitro, while knockdown of PAFR inhibited the effect of PAF on prostate cancer cells. We further found that PAFR promoted prostate cancer cell growth and metastasis invivo. Moreover, we found that PAFR activation increased MMP-3 expression and decreased E-cadherin expression of prostate cancer cells invitro and invivo. Finally, we found that PAFR time-dependently induced activation of ERK1/2, and ERK1/2 pathway contributed to PAFR-mediated prostate cancer cell invasion, migration and growth. Together, our findings demonstrate that PAFR can activate ERK1/2 pathway, and subsequently increase MMP-3 expression and decrease E-cadherin expression, which finally promote prostate cancer cell growth, invasion and metastasis. Thus, PAFR may act as a potential target for therapeutic use of prostate cancer.