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. 2024 Feb 20;5(2):101415. doi: 10.1016/j.xcrm.2024.101415

Figure 2.

Figure 2

MerTK promotes anti-PD-L1 resistance by suppressing ferroptosis in HCC

(A) All the differential genes between Hepa1-6 and Res1-6 cells were analyzed using KEGG pathway analysis using the functional gene sets in MSigDB (literature vs. databases containing signaling pathways).

(B) Fluorescence detection of lipid ROS by C11-BODIPY (left) and statistical analysis of relative lipid ROS fluorescence signal (right).

(C) Fluorescence detection of dead cells by SYTOX Green (left) and statistical analysis of percentage dead cells (right).

(D–F) Cell viability of Hepa1-6, Hepa1-6-OE-MerTK, Res1-6, and Res1-6-sh-MerTK strains treated with erastin (5.0 μM) in cocultured condition (left) and statistical analysis of cell survival rate in each time point (right).

(G–J) In subcutaneous xenograft mouse model, the statistical analysis of relative lipid ROS and MDA content in Hepa1-6, Hepa1-6-OE-MerTK, Res1-6, and Res1-6-sh-MerTK strains treated with anti-PD-L1 or IgG.

All results are shown as mean ± SEM (n = 5). One- or two-way ANOVA was used to analyze the data; ∗∗p < 0.01 and ∗∗∗p < 0.001.