Research Paper Volume 16, Issue 17 pp 12252—12262

Upregulation of EFCAB7 after radiofrequency ablation promoting hepatocellular carcinoma metastasis and survival by regulating PARK7

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Figure 2. EFCAB7 enhanced HCC proliferation and inhibited apoptosis in vitro and in vivo. (A) RT-PCR analysis of EFCAB7 in four different HCC cell lines; (B, C) Western blot and qPCR detecting knockdown efficiency of EFCAB7 in Huh7 and Hep3B HCC cell line; (D) Representative images of Huh7 and Hep3B after EFCAB7 silencing in the same fields after 1, 2, 3, 4 and 5 days; (E) Tumor cell proliferation was detected by CCK-8 assays after 1, 2, 3, 4 and 5 days and normalized to D1. (n = 3); (F) Proliferation of stable silencing Hep3B and Huh7 cells was evaluated by MTT assay in 1, 2, 3, 4 and 5 days. (n=3); (G) Apoptosis rate of tumor cells after knocking down EFCAB7; (H) Cell cycle analysis after knocking down EFCAB7; (I) Hep3B tumor cells (4 × 106 cells per mouse, n = 10 for each group) were subcutaneously inoculated in BALB/c nude mice. The mice were sacrificed at 10 days. (J) The tumor volumes were also measured in different days after inoculation; (K) Tumor weight was measured at 10 days. one-way ANOVA and Student’s t-test were used to compare differences with continuous variables (*P < 0.05, **P < 0.01, ***P < 0.001).