Fig. 7: Sirt1 potentiates the anticancer effect of chemotherapy and EGFR TKI treatment against KrasG12D-induced lung tumorigenesis.
From: Oncogenic KRAS mutation confers chemoresistance by upregulating SIRT1 in non-small cell lung cancer
A Schematic of genetic manipulation of LSL-KrasG12D/+ and/or Sirt1co/co mice before and after adenoviral Cre administration. B PET images of mice between 22 and 23 weeks of age. All images were normalized to the same maximal standard uptake value (SUVmax) to facilitate the comparison of PET lesions. The yellow arrow indicates the tumor region. Cisplatin (7 mg/kg/1 time/week, i.p.) and erlotinib (15 mg/kg/2 times/week, i.p.) were administered beginning 13 weeks after Ad-cre virus injection. C Quantification of the tumor uptake value (SUVmax) and mean standardized uptake value (SUVmax) in the lung. Student’s t test, mean ± SEM; n = 6; *p < 0.05. D Representative H&E-stained lung sections from LSL-KrasG12D/+;Sirt1+/+ and LSL-KrasG12D/+;Sirt1co/co mice. The bars represent 800 μm. E Average tumor number per lung area in specimens collected from LSL-KrasG12D/+;Sirt1+/+ (n = 6) and LSL-KrasG12D/+;Sirt1co/co (n = 6) mice between 24 and 27 weeks. Student’s t test, mean ± SEM; n = 6; *p < 0.05. F Survival rates of LSL-KrasG12D/+;Sirt1+/+ (n = 6) and LSL-KrasG12D/+;Sirt1co/co (n = 6) mice following Cre induction (log-rank test). G Median survival times (days) and P values were calculated using the log-rank test and Gehan-Breslow-Wilcoxon test on the basis of Student’s t test, respectively.
