Skip to main content
. 2019 Apr;8(2):473–482. doi: 10.21037/tcr.2019.03.01

Figure 3.

Figure 3

RAPA inhibited the expression of NKG2D ligand on the STAT3 signaling pathway. (A,B) RAPA upregulated the activity of STAT3 and ERK in HL-60 and THP-1 cells. AML cells were exposed to 0.1 µg/mL RAPA for 24 h. Cell lysates were prepared and subjected to western blot assay for p-STAT3 (Tyr705 and Ser727), total STAT3 protein, p-ERK, and total ERK. The phosphorylated STAT3 and ERK in HL-60 cells (A) and THP-1 cells (B) were increased after the treatment of RAPA; (C) without changing the basic expression of NKG2D ligand, STAT3 specific inhibitor upregulated the expression of ULBP3. HL-60 cells were treated with 0.1 µg/mL RAPA, 0.25 µmol/L STAT3 VII inhibitor or 0.1 µg/mL RAPA +0.25 µmol/L STAT3 VII inhibitor for 24 h. The expression of NKG2D ligands was analyzed using flow cytometry. Results are reported as mean ± SD of the 3 independent experiments. *, P<0.05 vs. RAPA group. RAPA, rapamycin; AML, acute myeloid leukemia; SD, standard deviation.