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. 2019 Jan 10;43(3):1382–1394. doi: 10.3892/ijmm.2019.4057

Figure 5.

Figure 5

Pris enhances the apoptosis of Cis-induced lung cancer cells via the downregulation of miR-23a. (A) A549 and NCI-H446 cells were treated with Pris (0.25 µM) for 0, 6 and 12 h. Relative expression levels of miR-23a were measured using reverse transcription-quantitative polymerase chain reaction analysis. Data are presented as the mean ± standard deviation of three independent experiments. **P<0.01, ***P<0.001, ****P<0.0001 vs. control. (B) A549 and NCI-H446 cells were transfected with miR-23a NC or inhibitor for 48 h. Western blotting was used to detect the protein expression of PTEN, p-Akt, Akt, p-GSK3β and GSK3β. β-actin served as a loading control. (C) A549 and NCI-H446 cells were transfected with miR-23a NC or inhibitor for 48 h, followed by treatment with or without Cis (20 µM) for 24 h. Cell apoptosis was analyzed using flow cytometry. (D) Graphs showing results of flow cytometry. Data are presented as the mean ± standard deviation of three independent experiments. **P<0.01. Cis, cisplatin; Pris, pristimerin; PTEN, phosphatase and tensin homolog; miR, microRNA; NC, negative control; GSK, glycogen synthase kinase 3β; p-, phosphorylated; PI, propidium iodide.