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. 2016 Jun 29;7(31):50117–50130. doi: 10.18632/oncotarget.10319

Figure 5. SIRT3 overexpression regulated GSTP1/JNK signaling pathway.

Figure 5

A. SIRT3 inhibited GSTP1 mRNA level. Forty-eight hour after lentivirus infection, SMMC-7721, Huh-7 and PLC/PRF/5 cells were treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml) for 48 h. The mRNA level of GSTP1 was detected by qPCR. β-actin mRNA expression was used as an internal control. B. SIRT3 inhibited GSTP1 protein level. The protein level of GSTP1 in SMMC-7721, Huh-7 and PLC/PRF/5 cells with or without chemotherapeutic agents was determined by western blot analysis. GAPDH was used as a loading control. C-E. The expression of total JNK, total c-Jun, phosphorylated-JNK, phosphorylated-c-Jun and Bim were examined in SMMC-7721 (C), Huh-7 (D) and PLC/PRF/5 (E) cells treated with doxorubicin (1 μg/ml), cisplatin (1 μg/ml) or epirubicin (0.5 μg/ml). GAPDH was used as a loading control. F. SIRT3 decreased the amount of GSTP1 that was associated with JNK. Immunoprecipitation was conducted with lysates prepared from SIRT3-overexpressing HCC cells (SMMC-7721 and Huh-7) or control cells treated with doxorubicin (1 μg/ml) by anti-JNK antibody, and immunoblotting was performed with anti-GSTP1 antibody.