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Fig. 4 | BMC Cancer

Fig. 4

From: Exosomal lncRNA HOTAIR induce macrophages to M2 polarization via PI3K/ p-AKT /AKT pathway and promote EMT and metastasis in laryngeal squamous cell carcinoma

Fig. 4

Exosomal lncRNA HOTAIR polarized the M2macrophage via down-regulating PTEN expression and activating a PI3K signaling pathway. Macrophages were incubated with exosomes extracted from TU212 cells or TU177 cells for 48 h, PTEN, PI3K and AKT in macrophage were tested by performing RT-PCR. B PTEN, PI3K and AKT protein in macrophage incubated with exosomes of TU212 cells and TU177 cells were performed by using WB. Original gels are presented in Supplementary Fig. 4-B-AKT, Fig. 4-B-PI3K, Fig. 4-B-PTEN, Fig. 4-B-β-actin (AKT), Fig. 4-B-β-actin (PI3K) and Fig. 4-B-β-actin (PTEN). C RT-PCR for CD206 and CD163 mRNA were measured in macrophage transfected with lncRNA HOTAIR mimics, post-transfected with PI3K inhibitor LY294002 and si-lncRNA HOTAIR inhibitor. Macrophages were transfected with lncRNA HOTAIR mimics, PTEN, p-AKT, and AKT protein in macrophage were detected by WB. D and E Macrophages were transfected with lncRNA HOTAIR mimics and post-treated with PI3K inhibitor LY294002, the differential expressions of PTEN, p-AKT, and AKT protein were quantified by performing WB. Original gels are presented in Supplementary Fig. 4-D-AKT, Fig. 4-D-PI3K, Fig. 4-D-p-AKT, Fig. 4-D-β-actin (AKT), Fig. 4-D-β-actin (PI3K) and Fig. 4-D-β-actin(p-AKT). Original gels are presented in Supplementary Fig. 4-E-AKT, Fig. 4-E-PI3K, Fig. 4-E-p-AKT, Fig. 4-E-β-actin (AKT), Fig. 4-E-β-actin (PI3K) and Fig. 4-E-β-actin (p-AKT). F Macrophages were transfected with si-lncRNA HOTAIR inhibitor, the differential expressions of PTEN, p-AKT, and AKT protein were detected by performing WB. Original gels are presented in Supplementary Fig. 4-F-AKT, Fig. 4-F-PI3K, Fig. 4-F-p-AKT, Fig. 4-F-β-actin (AKT), Fig. 4-F-β-actin(PI3K) and Fig. 4-F-β-actin (p-AKT)

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