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 4. Bcl-2 is the target of miR-129 in SAHA-tolerant NPC cells. (A) The WB of indicated proteins in SAHA-tolerant C666-1 and CNE-1 cells. (B) The mRNA level of Bcl-2 in SAHA-tolerant C666-1 and CNE-1 cells. (C) The expression of indicated proteins in C666-1 cells treated with miR-129 antagomir. (D) The Bcl-2 mRNA level in C666-1 and CNE-1 cells transfected with miR-129 antagomir. (E) The Bcl-2 expression in SAHA-tolerant C666-1 cells treated with miR-129 mimic. (F) The Bcl-2 mRNA level in SAHA-tolerant C666-1 and CNE-1 cells treated with miR-129 mimic. (G) The Bcl-2 reporter luciferase activity in C666-1 cells treated with miR-129 mimic. (H) The Bcl-2 mRNA level in 42 pair of adjacent tissues and primary NPC tumors. The Y-axis is on a linear scale. (I) The correlation of Bcl-2 and miR-129 expression in 42 NPC patient tumors. R2=0.1816. Each experiment was performed for 3 times. N, p>0.05; *, p<0.05; **, p<0.01; p<0.001.