Fig. 7
Suppression of ST8SIA6-AS1 restores the sensitivity of KRASG12Ci in vivo. A MIA PaCa-2-R cells were inoculated to form xenografts in nude mice (n = 5 mice/group). The administration dose and time of the drugs were recorded. B RTV of MIA PaCa-2-R xenografts treated with vehicle, MRTX849 and ST8SIA6-AS1 siRNA, alone or in combination. Tumor weights were measured after surgical resection. Data are the mean ± SEM (5 mice/group). *P < 0.05, **P < 0.01, and ***P < 0.001 by one-way ANOVA with Tukey’s multiple comparison test. C Changes in tumor volumes of individual mice in MIA PaCa‑2-R xenografts at the end of treatment. D Mouse body weights in MIA PaCa-2-R xenograft model were measured every 3 days during the experiments. Data are the mean ± SD. Statistical significance was assessed using two-tailed unpaired Student’s t test. *P < 0.05, **P < 0.01, ***P < 0.001. E Western blot analysis of tumor tissues at the end of the treatment. See also Additional file 2: Fig. S6. F Schematic model depicting the mechanism by which concurrent targeting of ST8SIA6-AS1/PLK1/c-Myc axis with KRAS elicits significant KRASG12Ci-resistant cell death