Fig. 7

HMGCR-induced cholesterol accumulation contributes to the role of ATG7 in colorectal cancer. (A-D) Serum cholesterol, TG, ALT and AST levels of MC38 tumor mice. (E) Representative oil red staining for tumor tissues (400×magnification). (F) The mRNA expression levels of the key genes of cholesterol metabolism upon treatment of ATG7 inhibition in CRC cells were measured by qRT-PCR. (G) The expression of HMGCR in TCGA COAD/READ cohort identified by GEPIA2. (H) The correlation between ATG7 and HMGCR in TCGA COAD/READ cohort. (I) IHC staining with antibody against HMGCR and quantification of relative intensity of HMGCR staining in MC38 xenografts treated with ATG7 inhibition (400×magnification). (J) The HMGCR protein level in shATG7-MC38 xenografts was analyzed by western blot. (K) TIP analysis was used to determine the correlation between HMGCR and T cell recruiting or infiltration of immune cells. (L-M) Tumor growth curves (L) and tumor burdens (M) of MC38 xenografts treated with shNC, shATG7 or atorvastatin combined with IgG or anti–PD-1 mAb (n = 5). (N) CD8 protein expression was examined by immunohistochemical analysis (400×magnification). Data are presented as the mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001