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. 2013 Dec 19;7(3):674–678. doi: 10.3892/ol.2013.1768

Figure 2.

Figure 2

Effect of AKR1C2 expression on cisplatin IC50 values in parental and HT1376-CisR cells. Cells were treated with various cisplatin concentrations for 72 h, and then quantified using a cell counter. Each assay was performed in triplicate. Cell survival in the absence of cisplatin was set as 100%. (A) Silencing AKR1C2 restored HT1376-CisR cell response to cisplatin. (B) Inhibition of AKR1C2 by 100 μM 5β-cholanic acid restored the HT1376-CisR response to cisplatin. *P<0.05, vs. HT1376-CisR. Bars indicate standard deviation. AKR1C2, aldo-keto reductase family 1 member C2; CisR, cisplatin-resistant.