Fig. 7: CAFs-derived CXCL5 reinforces exosomal HSPC111 excretion in CRC cells and promotes CRLM progression. | Cell Death & Disease

Fig. 7: CAFs-derived CXCL5 reinforces exosomal HSPC111 excretion in CRC cells and promotes CRLM progression.

From: Cancer-derived exosomal HSPC111 promotes colorectal cancer liver metastasis by reprogramming lipid metabolism in cancer-associated fibroblasts

Fig. 7

Western blot showed the protein levels of HSPC111, CXCR2 and EMT-relative genes in CAFs CM-incubated HCT116 (A) and SW480 cells (B). Migration of HCT116 (C) and SW480 cells (D) were analyzed by transwell assay after CAFs CM treatment. Scale bar = 200 μm. Western blot showed the protein levels of HSPC111, CXCR2 and EMT-relative genes in CAFs CM- and CXCL5 neutralizing antibody-incubated HCT116 (E) and SW480 cells (F). G Migration of HCT116 cells were analyzed by wound-healing assay after CAFs CM and CXCL5 neutralizing antibody treatment. Scale bar = 100 μm. Western blot showed the protein levels of HSPC111, CXCR2 and EMT-relative genes in CAFs CM- and CXCR2 inhibitor (navarixin)-incubated HCT116 (H) and SW480 cells (I). J Migration of HCT116 cells were analyzed by wound-healing assay after CAFs CM and CXCR2 inhibitor (navarixin) treatment. Scale bar = 100 μm. K IVIS imaging on experimental liver metastasis of indicated mice treated with ExoHCT116 KD or their relative control and with/without navarixin. Luciferase-labeled HCT116 cells were used to perform experimental liver metastasis model (n = 3). L Representative pictures and quantitative results of HE staining of liver tissue sections from indicated mice. Scale bar = 500 μm. Each experiment was performed in triplicate. Data are shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001.

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