Fig. 6: ENO1-RRM2 axis modulate deoxycytidine synthesis and promote gemcitabine resistance in pancreatic cancer.

In PANC-1 cells, ENO1 was knocked down (A), and in SW1990 cells, ENO1 was overexpressed (B). Subsequently, RRM2 was either knocked down or overexpressed, and dCTP levels were measured. analyzed using a two-tailed Student’s t-test. C, D. Representative fluorescence images and quantitative statistical analysis of γ-H2AX foci in PANC-1 cells after knocking down ENO1 and adding dCTP or overexpressing RRM2, induced by gemcitabine (5 μM, 24 hours) (C). In SW1990 cells, after overexpressing ENO1 and adding RRM2 inhibitor (3AP) or knocking down RRM2, induced by gemcitabine (2 μM, 24 h) (D). Data are analyzed using a two-tailed Student’s t-test. E, F. CCK8 assay to detect gemcitabine sensitivity in PANC-1 cells after knocking down ENO1 and adding dCTP or overexpressing RRM2 (E), and in SW1990 cells after overexpressing ENO1 and adding RRM2 inhibitor (3AP) or knocking down RRM2 (F).analyzed using a two-tailed Student’s t-test. G, H. Apoptosis rate and corresponding statistical graph in PANC-1 cells after knocking down ENO1 and adding dCTP or overexpressing RRM2, induced by gemcitabine (5 μM, 24 h) (G). In SW1990 cells, after overexpressing ENO1 and adding RRM2 inhibitor (3AP) or knocking down RRM2, induced by gemcitabine (2 μM, 24 h) (H). Data are analyzed using a two-tailed Student’s t-test. I. Schematic diagram of the mechanism by which ENO1-mediated upregulation of RRM2 promotes gemcitabine resistance in pancreatic cancer.All in vitro experiments were carried out in three replicates.