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. 2012 Oct;343(1):157–166. doi: 10.1124/jpet.112.195206

Fig. 6.

Fig. 6.

Role of CBR activation in the antiproliferative action of MNF in HepG2 cells. A, total RNA was extracted from HepG2, 1321N1, and U87MG cells, and then analyzed semiquantitatively by PCR. A nontemplate control (NTC) has been included (lane 1). GAPDH, glyceraldehyde-3-phosphate dehydrogenase. B and C, serum-depleted HepG2 cells were incubated with the CBR agonist WIN 55,212-2 (Win; 1 μM) (B) or antagonists AM251 (1 μM) or AM630 (0.5 μM) (C) for 1 h followed by the addition of vehicle, Fen (0.5 μM), or MNF (0.25 μM) for 24 h. D, serum-depleted HepG2 cells were pretreated without or with pertussis toxin (PTX; 50 ng/ml) for 16 h followed by the addition of vehicle, Fen (0.5 μM), MNF (0.5 μM), or WIN 55,212-2 (0.5 μM) for 24 h. In B to D, the levels of [3H]thymidine incorporation were measured. Quantification of percentage change in [3H]thymidine incorporation versus control is expressed as means ± S.D. and represents results from three (B and C) or two (D) independent experiments, each performed in triplicate dishes. *, p < 0.05.