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Fig. 7 | Journal of Hematology & Oncology

Fig. 7

From: Hepatic NOD2 promotes hepatocarcinogenesis via a RIP2-mediated proinflammatory response and a novel nuclear autophagy-mediated DNA damage mechanism

Fig. 7

Both RIP2 and lamin A/C are required for NOD2 activation-promoted hepatocarcinogenesis. a, b Male Lamnhep and Rip2/Lamnhep mice were injected with DEN (25 mg/kg, i.p.) at the age of 14–16 days followed by 8 injections of CCl4 (1.2 ml/kg, i.p., biweekly, starting 4 weeks after DEN injection) and either MDP (100 μg/mice, every other day) or PBS via intraperitoneal injection for 10 times starting three week before the first injection of CCl4. Mice were killed 1 and 6 months after DEN injection. a Representative immunohistochemistry images and quantification of 8-OHdG and γ-H2AX in livers of Lamnhep and Rip2/Lamnhep mice 1 month after DEN treatment. Arrowheads indicate γ-H2AX+ cells, n = 5. Scale bar, 50 μm or 25 μm. b Representative gross appearance, quantification of tumor number and size 6 months after DEN treatment are shown, n = 5–8. Arrowheads indicate tumors in liver. c Immunohistochemistry staining and semi-quantification of lamin A/C in HCC samples from ZHH1. n = 141. Scale bar, 50 μm. d Representative immunohistochemistry images of lamin A/C in HCC and ANT tissues. Scale bar, 50 μm. e Negative correlation between NOD2 and lamin A/C protein in HCC samples from ZHH1, n = 141; Pearson correlation analysis. Scale bar, 400 μm or 50 μm. f Allelic imbalances were measured in HCC clinical samples (red, AI; black, no AI). g Increased NOD2 expression in HCC patients from TCGA database with TP53 mutations. h Proposed schematic of hepatic NOD2 regulatory mechanisms in HCC carcinogenesis. Data were shown as mean ± SD, and significance was determined using ordinary two-way ANOVA with Sidak test (a, b), paired (c) and unpaired Student’s t test (g). *P < 0.05, **P < 0.01, n.s., not significant

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