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. 2016 Jul 21;7(34):54733–54743. doi: 10.18632/oncotarget.10752

Figure 4. Inverse association of MIR376A with MALAT1 expression in osteosarcoma tissues and direct interaction between MIR376A and the 3′UTR of MALAT1 in vitro.

Figure 4

(A) An inverse correlation between MALAT1 and MIR376A expression was observed. (B) Real-time PCR assay showed that knockdown of MALAT1 caused upregulation of MIR376A. (C) MALAT1 expression was decreased in response to MIR376A overexpression, compared with the MIR376A-NC group. Data are presented as mean ± SD of three independent experiments. (D) Generation of wt-MALAT1 and mut-MALAT1 containing luciferase reporter vectors by sequentially mutating the predicted MIR376A binding site in the MALAT1 3′ untranslated region. (E) The wt-MALAT1/mut-MALAT1 vectors and MIR376A-NC/MIR376A mimics were co-transfected into Saos2 cells, respectively. Luciferase activity of the wt-MALAT1 vector was reduced in cells co-transfected with MIR376A mimics. Repression of luciferase activity by MIR376A was not shown in cells transfected with mut-MALAT1. Data are presented as mean ± SD of three independent experiments.