Molecular mechanism of SHH-induced antiapoptotic signaling. Western blot analysis showing protein levels of (A) caspases and cleaved (c-) caspases and PARP in MM (ARP-1) cells in 24-hour cultures with or without the addition of BTZ (10 nM) or Mel (5 μM) in the presence or absence of aSHH (5 μg/mL) or rhSHH (50 ng/mL). (B) BCL-2 and cleaved PARP (c-PARP) in MM (ARP-1) cells treated with BTZ (10 nM) in the presence of different concentrations of aSHH (0 to ∼5 μg/mL) or rhSHH (0 to ∼5 ng/mL) for 24 hours. (C) GLI1 and BCL-2 in CAG, ^SHH–CAG, ^SHH+CAG cells, or ^SHH+CAG cells in the presence of aSHH (5 μg/mL), and CAG cells transfected with 2 μg of pBSU6-GLI1 short hairpin RNA (^Gli1–CAG) or pEGFP-GLI1 (^Gli1+CAG) plasmid for 48 hours. Percentages of apoptotic ARP-1 cells treated with (D) BTZ (10 nM) or with (E) Mel (5 μM) without or with BCL-2 inhibitor HA 14-1 (20 μM) and/or rhSHH (50 ng/mL) for 24 hours. Cell apoptosis was examined by Annexin-V binding assay. **P < .01.