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. 2019 Mar 8;10(20):1903–1917. doi: 10.18632/oncotarget.26726

Figure 4. STAT1 upregulation in MM cells by panobinostat in the presence of IFN-γ.

Figure 4

(A) STAT1 mRNA expression in MM cells. KMS-11, MM.1S and OPM-2 cells were cultured in triplicate for 24 hours with or without 25 nM of panobinostat in the presence or absence of 100 U/ml of IFN-γ. STAT1 mRNA expression was quantified by quantitative RT-PCR. Ratios of STAT1 over PPIE mRNA levels were calculated for a normalized target value (defined as 1). PPIE was used as an internal control. Results were expressed as the mean ± SD. *p < 0.05, **p < 0.01. (B) STAT1 and STAT3 expression in MM cells. KMS-11, MM.1S and OPM-2 cells were cultured for 6 or 24 hours with or without 25 nM of panobinostat in the presence or absence of 100 U/ml of IFN-γ. STAT1, STAT3 and PD-L1 mRNA expression was analyzed in the MM cells by RT-PCR. (C) Effects of STAT1 gene silencing on PD-L1 expression. STAT1 shRNA (clones #1 and #2) or control Luciferase shRNA were transfected into KMS-11 cells. The knockdown efficacy was examined by RT-PCR (left). The cells were cultured for 6 hours with or without 25 nM of panobinostat in the presence or absence of 100 U/ml of IFN-γ. PD-L1 mRNA expression was analyzed by RT-PCR. PPIE was used as an internal control. Pano, panobinostat.