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. 2022 Sep 23;12:963314. doi: 10.3389/fonc.2022.963314

Figure 1.

Figure 1

UA treatment inhibits cell proliferation and induces G2/M phase cell cycle arrest in cholangiocarcinoma cell lines. (A) Chemical structures of UA. (B) HuCCT-1 and SSP-25 cells were treated with UA at 0–80 μmol/L for 48 h Cell viability was measured using the Cell Counting Kit-8 assay. Data represent the means of three independent experiments. Bars, standard deviation; **P < 0.01. (C) HuCCT-1 and SSP-25 cells were treated with 0 or 40 μmol/L UA for 48 h Cell cycles were determined using flow cytometry. Data represent the means of three independent experiments. Bars, standard deviation; *P < 0.05; **P < 0.01. (D) HuCCT-1 were treated with 0, 10, or 40 μmol/L UA for 48 h Expression of cell cycle regulators was analyzed by Western blotting for phospho (p)-cdc2 (Try15), cyclin B1, and Cyclin D1. β-actin was used as internal loading control.