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

Figure 6

(a) Transwell analysis of MMP-3 overexpression group (MMP-3_OVER), normal control (NC_1), and MMP-3 silencing group (MMP-3_Si01) () under 10 μmol/L gemcitabine environment. (b) Spearman analysis of the association between NOX4 and MMP-3 in TCGA database. (c) NOX4 and MMP-3 expression in 20 μmol/L setanaxib treated high glucose, medium glucose, and low glucose group. (d) MMP-3 and NOX4 expression in 10 μmol/L H₂O₂ group, 20 μmol/L NOX inhibitor (setanaxib), 10 μmol/L NOX inhibitor (setanaxib), 10 μmol/L cordycepin, and normal control (NC_1). (e) Transwell analysis of 10 μmol/L H₂O₂ group, normal control (NC_1), and 20 μmol/L NOX inhibitor (setanaxib). (f) The cell viability of BxPc-3 cells treated with 50 μmol/L H₂O₂+10 μmol/L gemcitabine (GEM) group, 10 μmol/L H₂O₂+10 μmol/L GEM group, single 10 μmol/L GEM group, 5 μmol/L setanaxib+10 μmol/L GEM group, 10 μmol/L setanaxib+10 μmol/L GEM group, and 20 μmol/L setanaxib+10 μmol/L GEM group under different glucose groups (HG, MG, and LG). (g) The cell viability of BxPc-3 cells treated with 10 μmol/L GEM group, 10 μmol/L GEM+10 μmol/L cordycepin group, and 10 μmol/L GEM+20 μmol/L cordycepin group under different glucose groups (HG, MG, and LG).

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