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Fig. 3 | Journal of Hematology & Oncology

Fig. 3

From: Inhibition of bromodomain and extra-terminal (BET) proteins increases NKG2D ligand MICA expression and sensitivity to NK cell-mediated cytotoxicity in multiple myeloma cells: role of cMYC-IRF4-miR-125b interplay

Fig. 3

BETi increase susceptibility of MM cells to NK cell recognition and degranulation. a NK cells, prepared from PBMCs of healthy donors, were incubated with SKO-007(J3) cells, untreated or treated with the indicated BETi for 72 h as described above, and used as target cells in a degranulation assay. The assay was performed at the effector/target (E:T) ratio of 2.5:1. After 2 h at 37 °C, cells were stained with anti-CD56, anti-CD3, and anti-CD107a mAbs. Cell surface expression of CD107a was analyzed on FSC/SSC-gated and CD56+CD3 cells. In order to evaluate the role of NKG2D, the assay was performed in parallel treating NK cells with a blocking anti-NKG2D antibody. Percentage of CD107a positive cells was calculated based on five independent experiments and evaluated by paired Student t test (*P < 0.05). b BETi increase susceptibility of patient-derived MM PCs cells to autologous NK cell recognition and killing. CD138 bone marrow cells, cultured for 2 days in complete medium supplemented with IL-2 (200 U/mL), were incubated with purified autologous myeloma cells, untreated or treated with JQ1 for 48 h, and used as target cells in a degranulation assay. The assay was performed at the effector/target (E:T) ratio of 2.5:1. After 2 h at 37 °C, cells were stained with anti-CD56, anti-CD3, anti-CD16, and anti-CD107a mAbs. Cell surface expression of CD107a was analyzed on CD56+CD16+CD3 cells. Results obtained from two patients (P16 and P17) are represented

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