Figure 5.

Silencing of either JNK1 or JNK2 abolishes Bid phosphorylation in response to ALDH1L1 preventing both Bid accumulation and antiproliferative effects. (a) Levels of JNK1/2, Bid and their phosphorylated forms in PC-3 cells with silenced JNK2 upon ALDH1L1 expression. Silencing of JNK2 prevents ALDH1L1-induced cytotoxicity (b and c) and rescues PC-3 cells (c). Number of apoptotic cells (c) was calculated from annexin V assays shown in (b). (d) Levels of JNK1/2, Bid and their phosphorylated forms in PC-3 cells with silenced JNK1 upon ALDH1L1 expression. Silencing of JNK1 prevents ALDH1L1-induced cytotoxicity (e and f) and rescues PC-3 cells (f). Number of apoptotic cells in (f) was calculated from annexin V assays shown in (e). Differences between number of live cells at 72 h were highly statistically significant (indicated by *, P<0.0001 and <0.001 for c and f, respectively). Average of two independent experiments is shown for apoptotic cells; all MTT assays were performed with six replicates