FigureS 8 from Long-Chain Fatty Acid Redistribution Induced by SLC27A2 Deficiency Facilitates Hypoxic Adaptation and Immunosuppression in Hepatocellular Carcinoma

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Figure S8. Increased sensitivity of low SLC27A2-expressing HCC to glutaminase and fatty acid synthase inhibitors (A) Mechanistic illustration of FA metabolic vulnerability in SLC27A2^low HCC, reliant on glutamine's reductive metabolism and de novo FA synthesis. (B) Correlation between SLC27A2 expression and BPTES IC50 across HCC cell lines using GDSC data. (C) Random forest model constructed to predict BPTES sensitivity in an HCC bulk RNA dataset, based on median SLC27A2 levels. (D-F) Endogenous SLC27A2 abundance variability among HCC cell lines, noting HUH7's low expression profile. (G) SLC27A2 knockout effect on lipid raft formation in Li-7 cells. (H-L) SLC27A2 overexpression impact on HUH7 sensitivity to CB-839 (CB) and Orlistat (OR), ATP production, phospholipid levels, and membrane fluidity. Statistical methodologies: (M)Ki-67 assay for fig4S. Statistical techniques: Pearson correlation (B), one-way ANOVA with Tukey's test (E and M), Student’s t-test (J-L). *P < 0.05, **P < 0.01, ***P < 0.001

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