Skip to main content
Fig. 6 | Cell Communication and Signaling

Fig. 6

From: Acute myeloid leukemia-derived exosomes deliver miR-24-3p to hinder the T-cell immune response through DENN/MADD targeting in the NF-κB signaling pathways

Fig. 6

miR-24-3p promoted the development of Treg cells in AML. A Isolated Treg cells were cultured in the presence of Exo-miR-24-3p or Exo-anti-miR-24-3p for 5 days; Treg cells cultured in the medium were used as controls. The degree of apoptosis was measured by FACS (cells were labeled with annexin-V-FITC and PI). miR-24-3p-EXOs significantly decreased the apoptosis of Tregs compared with anti-miR-24-3p-EXOs (p < 0.0001). B CD4 + CD25 + Foxp3 + Tregs purified from HDs’ peripheral blood were transduced by the LV-miR-24-3p construct. Apoptosis was measured by FACS, and the overexpression of miR-24-3p decreased Treg apoptosis compared to the negative control (n = 5, *** p < 0.0002). C Western blot analysis of the expression level of phosphorylated proteins of the JAK/STAT signaling pathways: p-JAK3 and p-STAT5. D p-NF-κB and p-ERK in Treg cells after overexpression or inhibition of the miR-24-3p mimic. The overexpression of miR-24-3p by transfection of T cells with miR-24-3p mimic decreased the expression levels of p-NF-κB and p-ERK protein. The β-actin gene was included as a control. Representative data from three independent experiments are shown

Back to article page