Research Paper Volume 11, Issue 22 pp 10144—10153

Figure 5. LINC00899 directly binds to miR-425 in breast cancer. (A–B) Bioinformatic analysis of the potential miR-425 binding sites within wild-type LINC00899-1 (LINC00899 WT-1) or LINC00899-2 (LINC00899 WT-2). (C–D) Luciferase reporter vectors containing WT-1 (left) or WT-2 (right) as well as corresponding mutant (Mut, Mut-1 or Mut-2) miR-425 binding sequences were cotransfected into BC cell lines (MDA-MB-231 and SKBR3) together with miR-425 mimic or NC mimic. Dual-luciferase reporter assays were performed to assess the luciferase activity in MDA-MB-231 and SKBR3 cells expressing luciferase fused to WT-LINC00899 or Mut-LINC00899. (E) Spearman’s analysis of the correlation between LINC00899 and miR-425 levels in BC tissues. Data are presented as means ± SD, *p< 0.01. (F) Western blot analysis of DICER1, CDH1 and VIM expression in MDA-MB-231 and SKBR3 cells transfected with Lv-control, Lv-LINC00899 or Lv-LINC00899 plus miR-425 mimic. (G–H) qRT-PCR analysis of miR-425 and DICER1 expression in MDA-MB-231 and SKBR3 cells transfected with Lv-control or Lv-LINC00899. (I) Expression of LINC00899 in cells transfected with miR-control or miR-425 mimic. Data presented as means ± SD, *p< 0.01.