Fig. 3: CRC cell-derived exosomal HSPC111 alters lipid metabolism by increasing the level of acetyl-CoA in CAFs. | Cell Death & Disease

Fig. 3: CRC cell-derived exosomal HSPC111 alters lipid metabolism by increasing the level of acetyl-CoA in CAFs.

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

Fig. 3

A Bubble diagram of KEGG pathway enrichment analysis related to LX-2 cells incubated with ExoHCT116, compared with incubated with ExoHCT116 KD. B Heat map of significantly altered metabolites after HSCs incubated with ExoHCT116, compared with incubated with ExoHCT116 KD; p value < 0.05 are indicated. C Levels of acetyl-CoA and citrate in LX-2 cells incubated with ExoHCT116 KD and their relative control. D Levels of acetyl-CoA and citrate in LX-2 cells incubated with ExoSW480 OE and their relative control. E Normal fibroblasts (mNFs), non-tumoral fibroblasts (mNTFs) and cancer-associated fibroblasts (mCAFs) isolated from mouse liver tissues were photographed by light micrographs (top). Scale bar = 100 μm. Representative immunofluorescence staining of α-SMA and FAP in mNFs, mNTFs and mCAFs isolated from mouse liver tissues (bottom). Scale bar = 50 μm. Levels of acetyl-CoA and citrate in primary NFs, NTFs and CAFs isolated from human (F) and mouse (G) liver tissues. 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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