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Figure 5. RCC1 knockdown enhances the antitumor effects of 5-FU or Doxo in vivo. (A) Schematic overview of the experimental design. Drug-resistant CRC cells were subcutaneously injected into nude mice, followed by systemic drug administration after tumor formation. Mice were randomly divided into four groups. For the 5-FU-resistant group: scr + PBS (n = 5), sh3 + PBS (n = 5), scr + 5-FU (n = 5), sh3 + 5-FU (n = 5), (20 mg/kg, 3×/weeks for 2 weeks). For the Doxo-resistant group: scr + PBS (n = 5), sh3 + PBS (n = 5), scr + Doxo (n = 5), sh3 + Doxo (n = 5) (10 mg/kg cumulative, 1×/week); (B and C) Representative images of excised subcutaneous tumors in the 5-FU- or Doxo-resistant models after treatment; (D) Tumor volume measurements during treatment (two-way ANOVA); (E) Final tumor weights across all groups (one-way ANOVA); (F) Representative H&E staining of tumor sections from each group. Scale bar: 50 μm; (G) Ki-67 immunohistochemistry (left) and quantification of Ki-67-positive cells (right) using ImageJ (one-way ANOVA). Scale bar: 50μm; (H) TUNEL staining (left) and quantification of apoptotic cells (right) across groups. Scale bar: 50 μm; (I) Body weight monitoring of mice during treatment to assess tolerability (two-way ANOVA). ns, not significant; ^***P < 0.001; ^**P < 0.01; ^*P < 0.05. RCC1: Regulator of chromosome condensation 1; 5-FU: 5-fluorouracil; Doxo: doxorubicin; CRC: colorectal cancer; PBS: phosphate-buffered saline; scr: scramble; ANOVA: analysis of variance.