Fig. 6

NOP56 knockdown plus rapamycin inhibits KRAS-mutant tumor growth. A, Growth curve of xenograft tumors derived from H460 cells expressing either a control or an shRNA against NOP56 (shNOP56a). Rapamycin (0.1 mg/kg) was administrated i.p. for 3 weeks (5 days/week). Data are shown as mean ± SD). ***P < 0.001, *P < 0.05 and ns (P>0.05) by two-way ANOVA with Tukey’s multiple comparisons test. B, Relative tumor volume of H460 xenograft tumors after the treatment for 3 weeks. C, Weights of H460 xenograft tumors after the treatment for 3 weeks. ***P < 0.001 by one-way ANOVA with Tukey’s multiple comparisons test. D, Growth curve of xenograft tumors derived from H358 cells expressing either a control or an shRNA against NOP56 (shNOP56a). **P < 0.01 by two-way ANOVA with Tukey’s multiple comparisons test. E, Kaplan-Meier survival curve of mice with H358 xenografts from the experiment in D. F, Growth curve of PDX tumors derived from primary KRAS-mutant PF139 lung cancer cells expressing either control or NOP56-specific shRNAs. Data are shown as mean ± SD). ***P < 0.001 and *P < 0.05 by two-way ANOVA with Tukey’s multiple comparisons test. Immunoblots of PF139 cells expressing NOP56-specific or scrambled shRNAs was also shown. G, Relative tumor volume of PF139 xenografts after 3 weeks of treatment. H, Weights of PF139 xenograft tumors after treated for 3 weeks. ***P < 0.001, *P < 0.05 and ns P>0.05 by two-way ANOVA with Tukey’s multiple comparisons test. I, H&E and IHC of p-AKT(T308), p-mTOR(S2448), p-S6(S235/236), Ki67 and Caspase-3) in PF139 xenograft tumors after the treatment. Scale bars 100 μm