Fig. 4: Compositions and phenotypes of CAFs and EPCs in primary CRC and liver metastases. | Cell Discovery

Fig. 4: Compositions and phenotypes of CAFs and EPCs in primary CRC and liver metastases.

From: A single-cell atlas of liver metastases of colorectal cancer reveals reprogramming of the tumor microenvironment in response to preoperative chemotherapy

Fig. 4

a The percentage of CAFs in six primary CRC and six matched liver metastasis samples from six CRC patients with liver metastatic disease. Each dot represents one sample. *P = 0.031, two-sided Wilcoxon rank-sum test. b t-SNE plot showing a total of 1383 fibroblasts that can be separated into nine subtypes. Cells are colored according to different cell types (left), tissue origins (right, top), and treatment status (right, bottom). c Heat map showing the selected marker genes in each cluster. Relative expression was defined as the gene-wise (row) z-score of normalized UMI counts across CAF subtypes (column). d Box plots showing the percentage of each CAF subtype in primary CRC tumors treated with or without PC. Wilcoxon rank-sum test was used for statistical analysis. e GO analyses of genes that are differentially expressed between CAFs from tumors treated with PC and those from treatment-naïve tumors. Benjamini-Hochberg-corrected P values < 0.01. f Reclustering of EPCAM+ cells, colored according to clusters, sample origins, tissue origins, and treatment status. g t-SNE plots showing representative marker genes of EPCs. h GO analysis of genes that are differentially expressed between primary CRC and liver metastases in malignant cells. Selected GO terms with Benjamini-Hochberg-corrected P values < 0.05 (one-sided Fisher’s exact test).

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