Fig. 8

HCC patients exhibit PSTK overexpression that is correlated with the expression of GPX4. A Western blot showed the effect of recovering PSTK/GPX4 expressions with PSTK overexpressing for 48 h on Punicalin-induced PSTK/GPX4 deficiency and cleavage of PARP. B-C CCK-8 assays (n=6) and LDH release assays (n=6) showed the rescue effect with PSTK overexpressing for 48 h on Punicalin induced cell death. D Western blotting revealed the recovery of GPX4 expression following GPX4 overexpressing or selenocysteine treatment (SEC, 5 μM) for 48 h in the context of PSTK-KO induced GPX4 deficiency. E-F CCK-8 assays (n=4) and LDH release assays (n=3) demonstrated the rescue effects associated with GPX4 overexpression or selenocysteine treatment for 48 h on PSTK-KO induced cell death under sorafenib treatment. *p<0.05; **p<0.01; ***p<0.001; Student’s t-test. G PSTK expression in 50 pathologically confirmed HCC tissues and paired normal liver tissue samples as assessed via immunohistochemical staining, with expression being scored as high (+++), intermediate (++), low (+), or negative (-). H PSTK/GPX4 expression in 50 HCC tissues and paired non-tumor tissues (Paired t-test, p<0.0001). I Typical immunohistochemical staining results for PSTK/GPX4 staining in HCC tissues and paired non-tumor tissues. Scale bar: 100 μm. J Pearson correlation analyses of the relationship between PSTK/GPX4 immunohistochemical scores in 50 HCC samples or normal tissue samples. K Kaplan-Meier curves demonstrating the relationship between high levels of PSTK/GPX4 co-expression and shorter time to recurrence following surgery. L Schematic overview of the proposed mechanism whereby PSTK protects HCC cells against ferroptosis