Research Paper Volume 12, Issue 4 pp 3594—3616

Figure 3. FAM83H-AS1 functions as a sponge for miR-136-5p. (A) Predicted binding site of miR-136-5p in the FAM83H-AS1 sequence and mutated nucleotides. (B, C) Overexpression of miR-136-5p repressed the luciferase activity in TNBC cells transfected with FAM83H-AS1-Wt assessed by luciferase reporter assays. (D) Relative FAM83H-AS1 expression in TNBC cells transfected with mimic control, miR-136-5p mimic, inhibitor control, or miR-136-5p inhibitor. (E) Relative miR-136-5p expression in TNBC cells transfected with si-control, si-FAM83H-AS1, pcDNA-control, or pcDNA-FAM83H-AS1. (F) qRT-PCR analysis of miR-136-5p expression in human TNBC and adjacent control tissues. (G) qRT-PCR analysis of miR-136-5p levels in TNBC cell lines MDA-MB-231, MDA-MB-436, and MDA-MB-468, and a control breast epithelial cell line MCF-10A. (H) RIP assay demonstrating the enrichment of FAM83H-AS1 and miR-136-5p. * p < 0.05 compared to controls.