Figure 5: Suppression of CCNL2-induced p53 reporter activation by PKC inhibitors. a. ras-NIH3T3 cells were co-transfected with pG13-Luc, SV40-Rluc and CCNL2 expression plasmid or control plasmid, cultured for 24 h, and then cultured in the presence of various inhibitors or control solvent DMSO (0.1%) for another 24h. The final concentrations used were as follows: SP600125, 20 μM; p38 MAP kinase inhibitor, 2 μM; geldanamycin, 20 nM; staurosporine, 2.5 nM; GF109203X, 2 μg/ ml; 3-ATA, 5 μM; olomoucine, 50 μM; K252a, 500 nM; parthenolide, 1 μM; HA14-1, 10 μM; Akt inhibitor, 4 μM. b, ras-NIH3T3 cells were co-transfected with pG13-Luc, SV40-Rluc, expression plasmid of dominant negative PKCα (PKCα-DN), dominant negative PKCε (PKCε-DN), dominant negative JNK (JNK-DN) or control empty plasmid and CCNL2 expression plasmid or control plasmid. Cells were cultured for 48 h and then luciferase activity was measured. The error bars represent SD. *, P< 0.05 and **, P < 0.01 versus vector control, Student’s t test.