[Corrigendum] Lentivirus‑mediated RNA interference of clusterin enhances the chemosensitivity of EJ bladder cancer cells to epirubicin in vitro

Figure 2.

Analysis of the role of CLU in chemotherapeutic resistance. (A) A Matrigel invasive assay demonstrated that LV-CLU-infected cells combined with epirubicin treatment had minimum invasiveness. Statistical analysis revealed a significant difference between the LV-NC and LV-CLU groups with epirubicin treatment (P<0.01) (n=5). (B) A wound healing assay was used to detect the migration ability of EJ cells after CLU knockdown. LV-NC- and LV-CLU-infected EJ cells were treated with or without epirubicin, respectively, for 22 h. LV-CLU-infected EJ cells had a greater migrating distance compared to LV-NC infected EJ cells which were almost confluent. A significant difference was observed between the two groups (P<0.05) (n=6). (C) A plate clone formation assay with or without epirubicin treatment is shown. The data demonstrated that CLU knockdown EJ cells combined with epirubicin treatment had a lower clone formation rate than the other groups (P<0.05) (n=3). (D) Effect of CLU knockdown on the cell cycle detected by flow cytometric analysis. CLU-silenced cells demonstrated G0/G1 phase arrest and G2/M and S-phase reduction. After treatment with epirubicin for 24 h, 98.3% cells were blocked in the G0/G1 phase in CLU knockdown EJ cells, while only 64.9% cells were blocked in the G0/G1 phase in LV-NC-infected cells. The difference was statistically significant. CLU, clusterin; LV-CLU lentivirus targeting CLU; LV-NC, lentivirus targeting negative control.