P0065 S100A16 promotes cell migration and invasion in prostate cancer in vitro via AKT and ERK cell signalling pathways

Abstract

<h3>Background</h3> Expression of S100A16, a member of the S100 calcium binding protein family, is elevated in many types of tumours and appears to be associated with tumour cell proliferation. <h3>Methods</h3> By use of human prostate cancer cells as the model system, we evaluated the functional roles and underlying pathways of S100A16 in the proliferation and migration of prostate cancer cells. <h3>Findings</h3> S100A16 was significantly overexpressed in both human prostate cancer tissues and cell lines compared with normal controls. Exogenously introduced overexpression of S100A16 significantly promoted invasion, migration, and proliferation in human prostate cancer cells in vitro; whereas silencing the expression of S100A16 showed the opposite effects. Furthermore, overexpression of S100A16 activated AKT and ERK and reduced levels of the tumour suppressors p21 and p27. Pharmacological inhibition of PI3-kinase and MAP kinase via LY294002 and PD98059, respectively, attenuated the clone formation and invasion of DU-145 cells induced by S100A16 overexpression. <h3>Interpretation</h3> Our findings suggest that S100A16 can promote human prostate cancer progression via AKT and ERK signalling pathways as well as cell cycle regulators p21 and p27. S100A16 may serve as a novel therapeutic target or diagnostic marker of human prostate cancer progression.