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 3. Mir-129 is the sponging target of NEAT1. (A) The expression of indicated LncRNA in parental and SAHA-tolerant C666-1 cells. (B) A specific biotin-marked miR-129 probe to successfully arrest NEAT1 in relation to NC group. NC was referred to the non-specific biotin-labeled probe. (C) DLR assay was conducted to identify the direct link of NEAT1 and miR-129 on the basis of their complementary sequences. The pMIR-REPORT constructs with WT and mutant NEAT1 fragment insert were used. (D) The miR-129 expression in C666-1 cells with lenti-NEAT1. (E) C666-1 cells were treated with control or NEAT1 plasmid with or without co-transfection of miR-129 mimic, followed by 4 μmol/L of SAHA treatment for 1 d. The apoptosis was investigated through HOECHST 33258 staining. (F) The cleaved Cas-3 in C666-1 cells treated in (E). (G) The miR-129 expression in C666-1 cells transfected with NEAT1 siRNA. (H) C666-1 cells were treated with control or NEAT1 siRNA, followed by 4 μmol/L of SAHA treatment for 1 d. Apoptosis was investigated through HOECHST 33258 staining. (I) The cleaved Cas-3 in C666-1 cells treated in (H). Each experiment was performed for 3 times. N, p>0.05; *, p<0.05; **, p<0.01.