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Fig. 6 | BMC Cancer

Fig. 6

From: Exosome-derived lnc-HOXB8-1:2 induces tumor-associated macrophage infiltration to promote neuroendocrine differentiated colorectal cancer progression by sponging hsa-miR-6825-5p

Fig. 6

lnc-HOXB8-1:2 induces infiltration and M2 polarization of TAMs by sponging hsa-miR-6825-5p to upregulate CXCR3 expression. A, Predicted binding sites among lnc-HOXB8-1:2, hsa-miR-6825-5p and CXCR3 was found using RNA22 database and Target Scan database. And luciferase activity was reduced remarkably in the 293 T cells transfected with the exogenous hsa-miR-6825-5p mimics, and the inhibitory activity of hsa-miR-6825-5p was lost when the binding sites were lost. B, TAMs had greater migration and invasion capability after being treated with LoVo-CgA-OE cells or CgA-OE Exo. Scale bar = 200 μm. C, The proportion of M2 macrophages (stained by CD68 and CD206) increased when TAMs was cocultured with LoVo-CgA-OE cells or CgA-OE Exo. D-G, The expression of lnc-HOXB8-1:2 (D, F) increased while hsa-miR-6825-5p (E,G) decreased in TAMs cocultured with LoVo-CgA-OE cells or CgA-OE Exo. H–K, CXCR3 expression was upregulated in TAMs treated with LoVo-CgA-OE cells or CgA-OE Exo. L-M, The CXCR3 expression was reduced in TAMs transfected with the exogenous hsa-miR-6825-5p mimics. **, P < 0.01; ***, P < 0.001; NC, negative control; OE, overexpress; CgA, chromogranin A; Exo, exosomes; TAMs, tumor-associated macrophages; WT, wild-type; MUT, mutant type

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