Fig. 5: CRC cell-derived exosomal HSPC111 promotes CAFs to secrete CXCL5. A-D LX-2 cells treated with HSPC111-silent and -enriched exosomes were subjected to RNA-seq. | Cell Death & Disease

Fig. 5: CRC cell-derived exosomal HSPC111 promotes CAFs to secrete CXCL5. A-D LX-2 cells treated with HSPC111-silent and -enriched exosomes were subjected to RNA-seq.

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

Fig. 5

Overlapping of genes resulting from comparison of downregulated genes in LX-2 cells incubated with ExoHCT116 KD and upregulated genes in LX-2 cells incubated with ExoSW480 OE (A). Heat map of transcriptome alterations after incubating LX-2 cells with ExoHCT116 KD and ExoHCT116 KD Ctrl (B). Heat map of transcriptome alterations after incubating LX-2 cells with ExoSW480 OE and ExoSW480 OE Ctrl (C). The relative mRNA level of CXCL5 was analyzed in a group of independent samples (D). Western blot showed protein level of CXCL5 in LX-2 cells incubated with ExoHCT116 KD (E) and ExoSW480 OE (F) and their relative control respectively. ELISA analysis of CXCL5 level in culture medium from LX-2 cells incubated with ExoHCT116 KD (G) and ExoSW480 OE (H) and their relative control respectively. Immunofluorescence staining of α-SMA, FAP and CXCL5 in LX-2 cells incubated with ExoHCT116 KD (I) and ExoSW480 OE (J) and their relative control respectively. Scale bar = 20 μm. Each experiment was performed in triplicate. Data are shown as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001, ns not significant.

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