Fig. 4: Uptake of exosomal CCT6A induces M2 polarization via activating PI3K-AKT signaling pathway. | Cell Death & Disease

Fig. 4: Uptake of exosomal CCT6A induces M2 polarization via activating PI3K-AKT signaling pathway.

From: Tumor-derived exosomal CCT6A serves as a matchmaker introducing chemokines to tumor-associated macrophages in pancreatic ductal adenocarcinoma

Fig. 4

A KEGG enrichment analysis of DEGs between Exosh-NC and Exosh-CCT6A group. B Detection of PI3K-AKT signaling in Control (an equal volume of saline without exosomes), Exosh-NC, and Exosh-CCT6A treated macrophages via western blotting (left). Quantification (right) of p-PI3K/PI3K and p-AKT/AKT levels. (n = 3). Two-way ANOVA analysis. C Detection of PI3K-AKT signaling in Control, BxPC-3-Exo from control cells (BxPC-3-ExoOE-NC), BxPC-3-Exo isolated from CCT6A-overexpressing cells (BxPC-3-ExoOE-CCT6A), or BxPC-3-ExoOE-CCT6A with PI3K inhibitor LY294002 administration (BxPC-3-ExoOE-CCT6A + LY294002) treated macrophages via western blotting (left). Quantification (right) of p-PI3K/PI3K and p-AKT/AKT levels. (n = 3). Two-way ANOVA analysis. D RT-qPCR of M2 and M1 markers in macrophages treated with different BxPC-3-Exo groups. (n = 3). Two-way ANOVA analysis. E Representative images of IF staining for CD68 (red) and CD163 (green) in macrophages treated with different BxPC-3-Exo groups. Scale bar, 20 μm. F Flow cytometry analysis for distribution of M2-type (CD11b+CD163+) and M1-type (CD11b+CD86+) macrophages after different BxPC-3-Exo treatments (left). Quantification (right) of M2-type and M1-type macrophages. n = 3. One-way ANOVA analysis. Data presented as mean ± SD. n.s. no significant, *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001.

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