Figure 6 | Cell Death & Disease

Figure 6

From: Silencing NKG2D ligand-targeting miRNAs enhances natural killer cell-mediated cytotoxicity in breast cancer

Figure 6

HDACis increase the expression of NKG2DLs by inhibiting members of the miR-17-92 cluster. (a) and (b) Flow cytometry analysis. HDACis SAHA and VPA upregulated the expression of MICA/B and ULBP2 in BCap37 cells in a dose-dependent manner. (c) Flow cytometry analysis. HDACis SAHA and VPA could not effectively upregulate the expression of MICA/B and ULBP2 in the human normal breast cell line HBL-100. (d) Quantitative PCR analysis. HDACis SAHA and VPA inhibited the expression levels of pri-miR-17-92, miR-20a, miR-20b, miR-93 and miR-106b in a dose-dependent manner. (e) BCap37 cells were treated with HDACis (100 nM SAHA or 400 μM VPA) or HDACis together with miR-20a mimics(50 nM) for 48 h. Flow cytometry analysis revealed that miR-20a overexpression could reverse HDACi-mediated MICA/B and ULBP2 upregulation. (f) BCap37 cells were treated with different concentrations of HDACis or HDACis together with miR-20a mimics for 48 h, and then a 4 h cytotoxicity assay was performed using NK cells as effector cells. The NK cells were pretreated with control mAb or anti-NKG2D mAb 1 h before the cytotoxicity assay. (g) A schematic diagram of the mechanisms under HDACi-mediated NKG2DLs upregulation. Error bars represent the S.D. obtained from three independent experiments. *P<0.05, **P<0.01, *** P<0.001

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