Cells which is likely to contribute to their epithelial-like morphology and reduced motility. Besides the recruitment of E-cadherin to the Arr-HSC cell membrane, its expression in these cells was increased when compared to the Ctrl-HSC cells . The amount of E-cadherin mRNA in the Arr-HSC cells was 1.9-fold 60.06 , and that of protein 1.6- fold 60.12 , both significantly higher than in control cells . Strong immunofluorescence signals for the mesenchymal marker vimentin were observed in some 1152311-62-0 individual Ctrl-HSC and Arr-HSC cells, but evident differences in these signals could not be detected between the cell lines . We next wished to determine the reason underlying the thin top cell layer formed by the Arr-HSC cells in the organotypic model, and set out to study tumor cell proliferation and apoptosis. The number of proliferating Ki-67-positive tumor cells was smaller, but not statistically significant, in the Arr-HSC than in the Ctrl-HSC 3D cultures , which is in agreement with our observation on reduced tumor cell proliferation in Arr-HSC xenografts . The TUNEL assay showed that the Arr-HSC cells underwent apoptosis more often than the control cells in the 3D model . Since the TUNEL assay also detects other types of cell death in addition to apoptosis, we wanted to confirm our finding by caspase-3 staining. We observed a similar and significant trend on increased apoptosis in Arr-HSC cells 1403254-99-8 although the increase was milder than the one in the TUNEL assay. In HSC-3 xenografts, however, only few TUNEL-positive cells were detected mainly in the keratinized central tumor areas . We have previously shown that recombinant arresten affects mitochondrial apoptosisrelated Bcl-family signaling molecules in microvascular endothelial cells . In the current experiment the pro-apoptotic Bax protein showed 1.9-fold 60.23 increase in the Arr-HSC cells relative to the Ctrl-HSC cells , whereas the anti-apoptotic Bcl-xL protein level concomitantly showed a decreased, although not statistically significant, trend to 0.8-fold 60.049 of the controls , thus shifting the balance towards a situation favoring apoptosis . To pursue the mechanisms underlying the altered behavior and morphology of Arr-HSC cells we performed measurements using electric cell-substrate impedance sensing , a
