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. 2024 Aug 5;75:103302. doi: 10.1016/j.redox.2024.103302

Fig. 2.

Fig. 2

FDX1 inhibits proliferation, migration, invasion and promote apoptosis of HCC cells in vitro. (A) CCK8 assay showed the proliferative curves of FDX1-overexpressing MHCC-97H, FDX1-knockdown PLC/PRF/5 and their control cells. (B) Colony formation assays were used to evaluate the proliferation ability of HCC cell lines with overexpression or knockdown of FDX1. (C) The proportion of HCC cells with FDX1 overexpression or knockdown in G0/G1, G2/M, and S phases of cell division was analyzed by flow cytometry. (D) The rate of apoptosis in HCC cells with FDX1 overexpression or knockdown and in their control cells was analyzed by flow cytometry. (E) Cytoskeleton of indicated HCC cells visualized by staining of F-actin with rhodamine-conjugated phalloidin. DAPI was used to stain the cell nuclei. Scale bars, 5 μm. (F) Wound healing assay showed the migration ability of MHCC-97HFDX1, PLC/PRF/5shFDX1-1, PLC/PRF/5shFDX1-2 and their control cells at 0 and 24 h. Scale bars, 50 μm. (G) Transwell invasion assay showed the invasion ability of MHCC-97HFDX1, PLC/PRF/5shFDX1-1, PLC/PRF/5shFDX1-2 and their control cells at 24 h. Scale bars, 50 μm. Data shown as mean ± SD of triplicate independent experiments. *P < 0.05; **P < 0.01; ***P < 0.001.