Fig. 9

SHCBP1 knockdown synergistically enhances the tumour-killing effects of DNA-damaging drugs in vivo. BALB/c nude mice (6 mice per group) were injected subcutaneously in both flanks with 5 × 10⁵ HeLa-LUC cells (stably expressing luciferase) that had been infected with shCtrl or shSHCBP1 lentivirus for 4–5 days, respectively. The tumour-bearing mice were given etoposide (15 mg/kg) or the normal saline (NS) through intraperitoneal injection every other day when the subcutaneous tumour reaching around 200 cm.³, and the mice were finally sacrificed 31 days after tumour inoculation (end point). A Schematic diagram of the whole process of the tumour-bearing mouse experiment. B, C In-vivo bioluminescence imaging (left: shSHCBP1, right: shCtrl) (B) and isolated subcutaneous tumours (C) of two groups of tumour-bearing mice at the end point (31 days after tumour inoculation) are shown. D, E mouse weight (D) and tumour growth curve (E) util the end point among the groups; Black arrows represent the time points of etoposide or NS intervention. Data are expressed as mean ± SD and analyzed by the two-way ANOVA test; *, P < 0.05; ***, P < 0.001; ****, P < 0.0001. F, G Average tumour radiance (p/sec/cm3/sr) (F) of shCtrl and shSHCBP1 groups were analyzed in NS and ETOP groups on days 21 and 31 after tumour inoculation. Tumour weight (G) of shCtrl and shSHCBP1 groups were analyzed in NS and ETOP groups at the end point. Data are expressed as mean ± SD, p values were determined by the paired t-test. **, P < 0.01; ***, P < 0.001; ****, P < 0.0001