Supplementary Figure 1 from Hypoxia-Induced Creatine Uptake Reprograms Metabolism to Antagonize PARP1-Mediated Cell Death and Facilitate Tumor Progression in Hepatocellular Carcinoma

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Supplementary Figure 1. Hypoxia-induced upregulation of SLC6A8 highly associates with parthanatos antagonism and tumor progression in HCC. (A-C) HCC cells were treated as described in Figure 1D, and immunofluorescence (A) and Western blotting (B, C) showed the nuclear translocation of AIF. Scale bars, 10 μm. (D) Cell proliferation was determined by CCK-8. (E) The histogram showed the number of up- and down-regulated DEGs in Huh7 and Hep3B cells according to RNA-seq. (F, G) TCGA database analysis revealed that SLC6A8 was upregulated in LIHC. (H) Recurrence-free survival probability of TMA samples based on SLC6A8 expression was determined via Kaplan-Meier analysis. (I) Correlations between SLC6A8 expression and clinicopathological parameters of the TMA samples. (J) Correlation analysis of SLC6A8 and HIF-2α expression in HCC patients based on TCGA database. (K) Western blot analysis was performed to examine the regulatory effect of HIF-2α on SLC6A8 expression. n = 3 independent experiments. Means ± SD are shown; *P < 0.05, **P < 0.01, ***P < 0.001, and ns indicates no significant difference.

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