Fig. 4
From: Co-targeting WIP1 and PARP induces synthetic lethality in hepatocellular carcinoma
WIP1 inhibition disrupts DNA damage repair by increasing H2AX phosphorylation. A Gene set enrichment analysis (GSEA) of the gene expression profiles in WIP1 high expression and WIP1 low expression human liver cancer tissues. Red indicates WIP1 high expression; blue indicated WIP1 low expression. B Tumor mutation burden (TMB) was compared between WIP1 high and low expression liver cancer tissues from TCGA database. The phosphorylation of H2AX at S139 (γH2AX) was measured via Western blotting in HCC cells after WIP1 knockdown (C) or GSK2830371 inhibition (D). The Comet assay was performed to detect the DNA double strand break of PLC/PRF/5 cells after WIP1 knockdown (E) or GSK2830371 inhibition (25 μM, 48 h) (F). CASP software was used to calculate Tail/Head DNA percent of every single cell. The foci of γH2AX was measured via immunofluorescence to evaluated the DNA damage levels of PLC/PRF/5 cells after WIP1 knockdown (G) or GSK2830371 inhibition (25 μM, 48 h) (H). And the numbers of foci per cell were counted and shown