Amarogentin Inhibits Liver Cancer Cell Angiogenesis after Insufficient Radiofrequency Ablation via Affecting Stemness and the p53-Dependent VEGFA/Dll4/Notch1 Pathway

Figure 2

Amarogentin inhibits angiogenesis by decreasing the liver cancer cell stemness induced by iRFA. (a) The VEGFA supernatant levels in normal liver cancer cells and iRFA treatment cells at 12 h, 24 h, and 48 h were detected by ELISA. (b, c) The mRNA and protein expression levels of VEGFA and CD133 in normal liver cancer cells and iRFA cells at 48 h were detected by WB and reverse transcription-polymerase chain reaction (RT-PCR) assays. (d) HUVECs were cultured with supernatant from normal liver cancer cells and iRFA cells at 48 h to observe tube formation (400x). (e, f) The mRNA and protein expression levels of CD133 in normal liver cancer cells, iRFA cells, and iRFA cells treated with amarogentin were detected by WB and RT-PCR assays. (g) The VEGFA supernatant levels in normal liver cancer cells, iRFA cells, and iRFA cells treated with amarogentin were detected by ELISA. (h, i) The protein, phosphorylation, and mRNA expression levels of p53, Dll4, and Notch1 in normal liver cancer cells, iRFA cells (48 h), and iRFA cells treated with amarogentin were detected by WB and RT-PCR assays. N = normal liver cancer; iRFA = iRFA cells; iRFA+A = iRFA cells with amarogentin treatment group ().

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