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. 2016 Aug 1;6(8):1681–1694.

Figure 2.

Figure 2

MiR-122 confers resistance to 5-FU treatment in hepatic carcinoma cells in vitro. (A) miR-122 expression was increased in HepG2 and SNU-449 cells as compared with vector control, and ectopically expressing miR-122 as determined by quantitative real-time PCR. The data are presented as the Mean ± S.D. of triplicate experiments. **P < 0.01 compared to vector cells. (B) miR-122- and vector-expressing cells were treated with increasing concentrations of 5-FU for 72 h. MTT assays showed sensitivity of cells to 5-FU treatment. (C) DNA fragmentation assays showed sensitivity of those cells to 5-FU treatment. (D) Western blot analysis showed that cleaved PARP was higher in miR-122-expressing cells than vector control cells after 5-FU treatment. (E) An miR-122 inhibitor decreased miR-122 expression in HepG2 and SNU-449 cells as determined by quantitative real-time PCR. The data are presented as the Mean ± S.D. of triplicate experiments. **P < 0.01 compared to control cells. (F and G) The miR-122 inhibitor-treated or control cells were subjected to increasing concentrations of 5-FU. MTT assays (F) and DNA fragmentation assays (G) showed increased sensitivity to 5-FU-induced apoptosis in the inhibitor-treated cells as compared with the control cells. (H) Western blot analysis showed that cleaved PARP was lower in miR-122-expressing cells than control cells after 5-FU treatment.