Abstract
Prostate cancer is the most common cancer in men and is often associated with distant metastasis in its later stages. Cell surface receptors called integrins function as adhesion molecules that mediate both cell adhesion and motility. The adipokine apelin has been implicated in cancer progression and metastasis. However, the mechanisms by which apelin regulates integrin production and metastasis in prostate cancer remain unclear. Here, we found that apelin and integrin αvβ3 expression levels were elevated in prostate cancer samples compared to those in normal individuals. Apelin stimulation enhances integrin αvβ3-dependent prostate cancer migration. The activation of STAT3 and inhibition of miR-8070 via the MAPK pathway mediate apelin-facilitated integrin synthesis and cell motility. Importantly, our in vivo study indicated that inhibiting apelin reduces integrin αvβ3 expression and prostate cancer metastasis. Our results suggest that the apelin/integrin axis is a novel therapeutic target for treating metastatic prostate cancer.