PMA-induced reduction in invasiveness is associated with hyperphosphorylation of MARCKS and talin in invasive bladder cancer cells

摘要: Protein kinase C (PKC) plays a critical role in signal transduction for variety of cell activation processes. Enhanced PKC activity is often found cancer cells that show marked invasive and/or metastatic potential. Thus, specific inhibitor may serve as tool to reduce or potential cells. We here phorbol 12-myristate 13-acetate (PMA), activator, also reduces invasiveness EJ transitional carcinoma PMA-induced reduction was parallel with inhibition motility. PMA neither induced E-cadherin expression nor augmented cell-matrix adhesion caused retraction microspikes from the rim and consequently rounding cellular rim, disappearance microfilaments cytoplasm. at 10(-7) M, which concentration motility completely inhibited, down-regulated over 5 hr after transient translocation membrane fraction. At same time, hyperphosphorylation MARCKS talin. During process movement, actin-binding proteins are cycle phosphorylation dephosphorylation. Once this interrupted, can no longer maintain dynamics cytoskeletal structure. suggest retention hyperphosphorylated state talin responsible mechanism(s) by produces inhibitory against