Fig. 3: AXL inhibition induces TNF-α expression and promotes STING-type I interferon pathway. | Cell Death & Disease

Fig. 3: AXL inhibition induces TNF-α expression and promotes STING-type I interferon pathway.

From: Targeting AXL induces tumor-intrinsic immunogenic response in tyrosine kinase inhibitor-resistant liver cancer

Fig. 3

A Gene Set Enrichment Analysis (GSEA) of transcriptomes of AXL-low versus AXL-high HCC patients from TCGA-LIHC; left - Biocarta and right - Hallmark. B ELISA quantification of secretory TNF-α in sorafenib-sensitive (Sen) and sorafenib-resistant (SoraRes) HepG2 cells upon sorafenib treatment. C ELISA quantification of secretory TNF-α in Sen and SoraRes HepG2 cells upon BGB treatment. D Representative FACS plots (top) and percentages (bottom-right chart) of mitoSOX staining in Sen and SoraRes HepG2 cells upon BGB324 treatment. E qRT-PCR quantification of mt16S, mtDloop, and mtCYTB levels in the cytosol extract of Sen and SoraRes HepG2 cells upon BGB324 treatment. F WB analysis of STING pathway in SoraRes HepG2 cells upon BGB324 treatment. G ELISA quantification of secretory IFN-α in Sen and SoraRes HepG2 cells treated with BGB324. H qRT-PCR quantification of ISGs in Sen and SoraRes HepG2 cells treated with BGB324. I GSEA of AXL-high versus AXL-low HCC patients from TCGA-LIHC showing a negative correlation with interferon-stimulated gene signature. *p < 0.05; **p < 0.01; ****p < 0.0001; n.s. not significant on a two-tailed unpaired Student’s t test or one-way ANOVA with Bonferroni’s multiple comparisons test.

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