Wada et al. [ 3] found that DEX inhibited PAN-induced podocyte apoptosis by downregulating the expression of p53, upregulating Bcl-xL, and delaying the translocation of apoptosis-inducing factor (AIF) from cytoplasm to nucleus.
Caspase 3 cleavage was not detected in infected cells and oncolysis was observed in pan-caspase inhibited cells.
In contrast to EGFR and Src inhibition, a pan-Jak inhibitor inhibited pJak2 and Stat3 phosphorylation.
Combined treatment with thioridazine and TRAIL increased caspase-3 activation, and z-VAD-fmk (z-VAD), a pan-caspase inhibitor, markedly inhibited thioridazine plus TRAIL-induced apoptosis.
We found that the pan-PKC inhibitor Calphostin C inhibited infection in both cell types similar to Rottlerin and Chelerythrine Chloride (Table 1).
Furthermore, the pan-caspase inhibitor zVAD-fmk inhibited IFN-γ-induced cell death, albeit only at high concentrations (Fig. 7).
In the current investigation the pan-caspase inhibitor ZVAD-fmk inhibited apoptosis induced by 3CPA both in 70Z/3 and HL60 cells.
Treatment of HeLa-CD95 cells (Supplementary Figure S5) and HeLa-CD95 cells overexpressing c-FLIPL or c-FLIPR (Supplementary Figure S6) with the pan-caspase inhibitor zVAD-fmk inhibited phosphorylation of ERK1/2 and p38.
Similarly, treatment the cells with the pan-caspase inhibitor (Z-VAD-FMK) totally inhibited DOX- or PTX-induced apoptosis.
Data shown in Figure 4 indicate that CCM and DHA, in varying concentrations of a fixed 2 3 ratio, inhibited cell proliferation in a dose dependent manner 20-900 μM), and the pan-caspase inhibitor significantly reduced the effect of CCM+DHA at all concentrations tested.
Moreover, blocking selectins with pan-inhibitor GMI-1070 in MM mouse model in combination with bortezomib inhibited tumor growth during treatment and delayed tumor progression after halting the therapy significantly improving mice survival [ 6].
