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 2. miR-129 downregulation contributes to SAHA tolerance in NPC. (A) The mRNA level of miR-129 in parental and SAHA-tolerant phenotype. (B) The relative level of miR-129 in 42 pair of adjacent tissue and primary NPC tumors. The Y-axis is on a linear scale. (C) The survival of NPC patients with different levels of miR-129. If the expression level was higher than the average value of miR-129 expression in primary tumors, the patients were grouped into high expression group (n=15). The left patients were grouped as miR-129 low expression patients (n=27). (D) C666-1 cells were subjected with control or miR-129 mimic, followed by 4 μmol/L of SAHA treatment for 1 d. The apoptosis was investigated through HOECHST 33258 staining. (E) The cleaved caspase-3 in C666-1 cells treated in (D). (F) The survival of C666-1 cells transfected with control or miR-129 mimic, followed by different concentrations of SAHA treatment. (G) C666-1 cells were transfected with control or miR-129 antagomir, followed by 4 μM SAHA treatment for 24 h. The apoptosis was analyzed through HOCHST 33258 staining. (H) The cleaved caspase-3 in C666-1 cells treated in (G). (I) The survival of C666-1 cells transfected with control or miR-129 antagomir, followed by different concentrations of SAHA treatment. Each experiment was performed for 3 times. *, p<0.05; **, p<0.01; p<0.001.