Fig. 6
ZNF498 functions as an oncogene in a p53-dependent manner. A, B, C HepG2 cells with stable overexpression (A) or knockdown (B) of ZNF498 and Hep3B cells with overexpression of ZNF498 (C) were cultured for CCK-8 and colony formation assays. ZNF498 expression was detected using Western blotting. D p53 reintroduction restored the promoting effect of ZNF498 on the growth of Hep3B cells. EV and ZNF498-overexpressing Hep3B cells were transfected with or without the p53 expression vector, and cell proliferation was measured using a CCK-8 assay. E p53 knockout diminished the promoting effect of ZNF498 on the growth of HepG2 cells. EV and p53-knockout HepG2 cells were transfected with or without the ZNF498 expression vector, and cell proliferation was measured using the CCK-8 assay. F-H A total of 1.5 × 106 HepG2 cells with or without overexpression of ZNF498 (F), 4 × 106 HepG2 cells with or without downregulation of ZNF498 (G), and 1.5 × 106 p53- knockout HepG2 cells with or without overexpression of ZNF498 (H) were injected into nude mice, which were then housed for different times. Tumors were isolated, and tumor weight and volume were measured. I, J The association between ZNF498 mRNA levels and OS in TP53 WT and TP53 mutated subgroups of patients with HCC was evaluated by Kaplan–Meier analysis. K, L Kaplan–Meier survival curves for p53-low and p53-high HCC patients, respectively. ns: no significance; **P < 0.01