Fig. 5

PMA or CM1 upregulated MMP-9 via the ERK, p38 MAPK and NF-κB pathways. a PMA (m ϕ CM) induced MMP-9 expression via activation of MAPK and NF-κB pathways. NPC cells were pre-treated with specific inhibitors of ERK 1/2 (U0126, 10 μM), p38 (SB203580, 10 μM), JNK (SP600125, 10 μM) or NF-kB (QNZ, 10 μM) for 1 h, then treated with PMA (100 nM) or m ϕ CM for 18 h, and MMP-9 levels in the CM were determined by gelatin zymography. The relative level of MMP-9 expression was compared in cells treated with MAPK or NF-κB inhibitor plus PMA and PMA treatment alone; N = 3, ^*P<0.05. b PMA induced the reporter activity of MMP-9 in NPC cells. NPC 039 cells were transfected with pGL-MMP9-Luc for 24 h. Transfected cells were treated with U0126, SB203580, or QNZ for 1 h, then exposed to PMA (100 nM) for 6 h. Luciferase activity is presented relative to the control group. c MAPK or NF-kB signaling was not directly involved in the regulation of the intracellular cleavage of N-cadherin. NPC cells were pretreated with the indicated inhibitors for 1 h before 8 h of PMA exposure. Cell lysates underwent immunoblotting with the indicated antibodies. The relative CTF1 accumulation was compared with the control group (PMA-untreated cells); N = 3, ^*P<0.05