Research Paper Volume 13, Issue 14 pp 18498—18514

Figure 3. M/T-Exo miRNA-205 enhances the tamoxifen resistance of breast cancer cells (BCCs) via targeting E2F1. (A) The putative sequence of miRNA-205 binding sites in the 3′UTR of E2F1. (B) Relative luciferase activity. (C) The expression of miRNA-205 in M/T-Exo-cocultured BCCs treated with DMSO or GW4869. (D–E) The mRNA and protein expressions of E2F1 in M/T-Exo-cocultured BCCs treated with the negative control miRNA-205 inhibitor (NCi), miRNA-205 inhibitor (205i), or the combination of 205i and lentiviral vector carrying E2F1 (E2F1). (F) Cell viability of M/T-Exo-cocultured BCCs treated with the negative control miRNA-205 inhibitor (NCi), miRNA-205 inhibitor (205i), or the combination of 205i and lentiviral vector carrying E2F1 (E2F1). (G–H) The mRNA and protein expressions of E2F1 in M/T-Exo-cocultured BCCs treated with DMSO or GW4869. (I) Cell viability of M/T-Exo-cocultured BCCs treated with DMSO or GW4869. (J–K) The mRNA and protein expressions of E2F1 in M/T-Exo-cocultured BCCs treated with the negative control miRNA-205 inhibitor (NCi), miRNA-205 inhibitor (205i), or the combination of 205i and E2F1 siRNA (siE2F1). (L) Cell viability of M/T-Exo-cocultured BCCs treated with the negative control miRNA-205 inhibitor (NCi), miRNA-205 inhibitor (205i), or the combination of 205i and E2F1 siRNA (siE2F1). Values are means ± SD. ^*P < 0.05, ^**P < 0.01, ^***P < 0.001. At least three replicates were available for analysis in each treatment group.