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. 2015 May 28;107(8):djv132. doi: 10.1093/jnci/djv132

Figure 3.

Figure 3.

Effect of CES2 knockdown and overexpression on pancreatic cancer cell irinotecan sensitivity. A) Western blot analysis of CES2 expression in: (left panel) Hs 766T, AsPC-1 and CFPAC-1 pancreatic cancer cell lines nontransduced (parental) and stably transduced with a shRNA targeting CES2 (CES2 KD) or a scrambled shRNA as a control (control); and (right panel) SU.86.86 pancreatic cancer cell line nontransduced (parental) and stably transduced with a lentiviral construct overexpressing CES2 (CES2 OE), and the respective empty vector as a control (control). β-actin was used as loading control. B) Quantitative real-time polyermase chain reaction analysis of CES2 transcript levels, C) relative CES2 activity, and D) relative half-maximal inhibitory concentration (IC50) of irinotecan in the above described pancreatic cancer cell lines after CES2 knockdown and overexpression. Results are the mean of three independent experiments ± SD (error bars) of triplicates. P values were calculated by two-sided unpaired t test. *P < .05, ** P < .01, *** P < .001 relative to parental cell lines. CES2 KD = CES2 knockdown; CES2 OE = CES2 overexpression; IC50 = half-maximal inhibitory concentration.