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. 2019 Jul 30;12:6083–6092. doi: 10.2147/OTT.S211560

Figure 2.

Figure 2

The inhibition of ATR reverses cisplatin-induced DDR. (A) Western blot and semiquantitative analysis of the levels of phosphorylated ATR and Chk1 in SW1353 cells treated with the indicated concentrations of VE-822 alone or VE-822 plus 10 μM cisplatin for 24 h. (B) Western blot and semiquantitative analysis of the levels of phosphorylated ATR and Chk1 in CS-1 cells treated with the indicated concentrations of VE-822 alone or VE-822 plus 10 μM cisplatin for 24 h. (C) Western blot and semiquantitative analysis of the levels of phosphorylated H2AX in SW1353 cells treated with the indicated concentrations of VE-822 alone or VE-822 plus 10 μM cisplatin for 24 h. (D) Western blot and semiquantitative analysis of the levels of phosphorylated H2AX in CS-1 cells treated with the indicated concentrations of VE-822 alone or VE-822 plus 10 μM cisplatin for 24 h. (E) Western blot and quantitative RT-PCR analysis of the levels of ATR in SW1353 cells transfected with ATR shRNA. ***P<0.001 compared with the control group. (F) Western blot and semiquantitative analysis of the levels of phosphorylated ATR and Chk1 in SW1353 cells transfected with ATR shRNA and cultured in the presence or absence of 10 μM cisplatin for 24 h. (G) Western blot and semiquantitative analysis of the levels of phosphorylated H2AX in SW1353 cell, transfected with ATR shRNA and cultured in the presence or absence of 10 μM cisplatin for 24 h.