Fig 7. Inhibition of ERK1/2 or JNK signaling suppresses the development of colon tumor in type 2 diabetes model.

2 × 10⁶ MC38 cells suspended in 0.1 ml of PBS were subcutaneously injected into the db/db mice to initiate tumor growth in vivo. 10 mg/kg PD98059 or 30 mg/kg SP600125 was administered intraperitoneally every 3 days when tumor volume reached 100mm³. 1% DMSO was used as control treatment. (A) Tumor size was measured every 3 days. *P<0.05; ***P<0.001. (B) The tumors were excised and weighted 3 weeks after cell injection. ***P<0.001. A representative tumor mass from each group was shown in the inset (scale bar = 1cm). (C and E) Western blotting analysis of p-ERK1/2, ERK1/2, p-JNK, JNK, Cyclin D1, Bcl-2, Bax and Caspase3 protein expression in tumors. GAPDH served as a loading control. The blots shown are representative of three separate experiments. (D and F) Semi-quantitation for the expressions of ERK1/2 and pERK1/2, JNK and p-JNK, Cyclin D1, Bcl-2, Bax and Caspase3 protein. Fold changes were normalized by control groups. **P<0.01; ***P<0.001 versus control, n = 3 per group.