Research Paper Volume 12, Issue 14 pp 14174—14188

LncRNA NEAT1/miR-129/Bcl-2 signaling axis contributes to HDAC inhibitor tolerance in nasopharyngeal cancer

Figure 5. Bcl-2 mediated the SAHA tolerance in NPC cells. (A) SAHA-tolerant C666-1 cells were transfected with control or Bcl-2 siRNA, followed by 4 μmol/L of SAHA treatment for 1 d. The cleaved Cas-3 expression was investigated via WB. (B) The apoptosis of C666-1 cells obtained in line with (A). (C) The survival of SAHA-tolerant C666-1 cells treated with control or Bcl-2 siRNA, followed by different concentrations of SAHA treatment. (D) C666-1 cells were subjected to control or miR-129 antagomir with or without co-transfection of Bcl-2 siRNA, followed by 4 μmol/L of SAHA treatment for 1 d. The cleaved Cas-3 expression was investigated via WB. (E) The apoptosis of C666-1 cells obtained in line with (D). (F) The apoptosis of SAHA-tolerant C666-1 cells treated with 4 μmol/L of SAHA with or without co-treatment of ABT-737 (2 μmol/L). (G) The apoptosis of SAHA-tolerant C666-1 cells treated with 4 μmol/L SAHA with or without co-treatment of ABT-263 (2 μmol/L). (H) The apoptosis of SAHA-tolerant C666-1 cells treated with 4 μmol/L SAHA with or without co-treatment of ABT-199 (2 μmol/L). Each experiment was performed for 3 times. **, p<0.01.