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. 2021 Jun 4;12(15):4661–4671. doi: 10.7150/jca.53115

Figure 7.

Figure 7

The deletion of ApoM gene accelerates the tumorigenesis rate of C57BL/6J mouse liver cancer induced by N-nitrosodiethylamine. (A) Livers were taken at 0, 4, 8, 12, 16 and 20 weeks. Compared with WT mice, ApoM gene-deficient mice developed tumors earlier under N-nitrosodiethylamine induction. (B) Western blot assay showed that the ApoM level in the cancer tissue of WT mice in the liver cancer induction model group was lower than that in the paracarcinoma tissues (P=0.010). (C) Compared with the WT group, the ApoM gene deletion group had higher wet liver weight per month. At 12 weeks, the wet liver weight of the ApoM gene deletion group was higher than that of the WT group and was statistically significant (P=0.0048). (D) The body weight of mice in the WT group increased from 0 weeks to 12 weeks, and their body weight decreased after 12 weeks. The body weight of mice in the ApoM gene deletion group increased from 0 to 8 weeks, and their body weight decreased after 8 weeks. (E, F) Liver function ALT (P=0.00013) and AST (P=0.00061) levels of liver cancer induction model ApoM-/- group are higher than those of WT group, and have statistical significance. (G) Western blot analysis of liver cancer induction model, the key apoptosis proteins Cleaved-caspase9 (P=0.20), Cleaved-caspase3 (P=0.26), Bax/Bcl-2 (P=0.014) in wild mice were higher than ApoM gene deletion group. (P=0.0011). (H) Compared with the WT group, the ApoM gene deletion group has a faster time for liver tumors, which was statistically significant (P=0.028). (I) The survival of ApoM-/- mice was shorter than that of WT mice (P=0.011).