fig1

Figure 1. c-Jun NH2-terminal kinase (JNK)-mediated phosphorylation of paxillin Ser178 plays a role in tumor cell migration. MTLn3 cells were either untreated or treated with EGF (10 nmol/L) in the absence or presence of the JNK inhibitor SP600125 (20 μmol/L). A: migration of these cells was observed by live DIC microscopy. Snapshots of the time-lapse made for 2 h are shown, scale bar is 50 μm. See movie M1; B: at 0, 5 and 10 min after treatment cells were fixed and stained for the nucleus (blue) and β-catenin (green). Scale bar is 20 μm; C: overall migration trajectories of individual cells of one representative experiment (only one position from the 6 technical replicates of one biological replicate); D: average cell speeds of about 100 cells per treatment imaged in one biological replicate were plotted. This graph shows the data for one representative biological replicate.*P < 0.05, **P < 0.01, ***P < 0.001; E: the JNK signaling pathway was analyzed by Western Blotting using the indicated antibodies. The arrows indicate the phospho specific bands of the different antibodies. The paxillin antibody detects also a paxillin family member leupaxin encoded by LPXN, which has a much lower molecular weight than paxillin encoded by PXN