High Glucose Promotes Pancreatic Ductal Adenocarcinoma Gemcitabine Resistance and Invasion through Modulating ROS/MMP-3 Signaling Pathway

Figure 1

(a) Different glucose groups (HG, MG, and LG) BxPc-3 cells treated with normal control (NC), single 10 μmol/L GEM group, single 20 μmol/L setanaxib, and single 20 μmol/L cordycepin. (b) Different glucose groups (HG, MG, and LG) BxPc-3 cells treated with single 10 μmol/L GEM group, 10 μmol/L setanaxib+10 μmol/L GEM group, and 20 μmol/L setanaxib+10 μmol/L GEM group, 10 μmol/L cordycepin+10 μmol/L GEM group, and 20 μmol/L cordycepin+10 μmol/L GEM group. (c) MMP-3 expression in natural generated gemcitabine resistant cell line (BxPc-3 (GemR)) and in normal control (BxPc-3 (Normal)). (d) The schematic diagram and the timeline of the in vivo experiment in nude mouse. (e) The cell viability of BxPc-3 (GemR) and BxPc-3 (Normal) after treated with10 μmol/L GEM, 20 μmol/L setanaxib+10 μmol/L GEM, and 20 μmol/L cordycepin+10 μmol/L GEM for 24 h. (f) The K-M survival plot of the mice in the GEM+cordycepin treated group, and single GEM treated group (). (g, h) Tumor volume comparison between GEM + cordycepin treated diabetic group and single GEM treated group ().

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