Figure 7.

A schematic diagram showing the mechanisms of TLK1 > MK5 signaling in promoting prostate cancer migration and invasion. Combined with our previous findings, TLK1-mediated phosphorylation of MK5 in three novel residues (S160, S354, and S386) may promote the shuttling of MK5 out of the nucleus, where it exerts its pro-metastatic function by modulating the phosphorylation of focal adhesion proteins (pFAK Y861 and pPaxillin Y118) and HSP27 (pHSP27 S82) that enhances actin filamentation and reorganizations in the leading edge of the cells. Furthermore, TLK1 > MK5–mediated ERK3 stabilization stimulates several MMPs’ (MMP2 and MMP9) expression, which enhances invasive capacities of the PCa cells. Co-ordinated effects of these signaling events finally orchestrate the functional metastasis of PCa cells.