Research Paper Volume 12, Issue 20 pp 20658—20683

Cross-talk between the ER pathway and the lncRNA MAFG-AS1/miR-339-5p/ CDK2 axis promotes progression of ER+ breast cancer and confers tamoxifen resistance

Figure 3. MAFG-AS1 promotes the progression of ER+ breast cancer through sponging miR-339-5p. (A) The expression of MAFG-AS1 was higher in cytoplasm than nucleus in T47D cells. (B) Expression of miR-339-5p in 50 breast tumors compared with para-carcinoma tissues *p<0.05. (C) Expression of miR-339-5p and MAFG-AS1 from 50 breast tumors were negatively correlated. (D) miR-339-5p expression after siMAFG-AS1-1, siMAFG-AS1-2 or NC-siRNA transfection in T47D and MCF-7 cells.18s was used as an internal control. (E) Bioinformatic analysis revealed the presence of complementary binding sites for miR-339-5p in MAFG-AS1. (F) Luciferase activity in T47D/MCF-7 cells cotransfected with miR-339-5p and luciferase reporters containing pmirGLO-MAFG-AS1-WT or pmirGLO- MAFG- AS1-MUT. (G) The expression of MAFG-AS1 and miR-339-5p after anti-Ago2 RIP were performed in T47D and MCF-7. IgG was used as a negative control. (H, I) MiR-339-5p overexpression abolished the cell proliferation induced by MAFG-AS1 shown by both MTT assay and colony formation assay. (J) Overexpression of MAFG-AS1 cells displayed a significantly low frequency of cells at G1 phase and a high frequency of cells at S phase, while miR-339-5p reversed it. (K) MiR-339-5p restored the MAFG-AS1 induced repressing of cell apoptosis.