Fig. 6: The landscape of epithelial cells and the cell–cell communication analysis.
From: Single-cell transcriptomic profiling reveals liver fibrosis in colorectal cancer liver metastasis

a A UMAP view of MCs and NCs (top) and cell density (bottom) demonstrating the distribution between Fibrosis+ LM and Fibrosis− LM. High relative cell density is shown as bright magma. b The violin plot compared the CNV scores of MCs between Fibrosis+ LM and Fibrosis− LM, Wilcox rank-sum test. c A heat map illustrating the expression profiles of curated gene signatures in MCs between the Fibrosis+ LM and Fibrosis− LM. The heat map is based on scaled gene signature scores, Wilcox rank-sum test, P value: **≤0.01, ***≤0.001. d A bar chart displaying the Augur scores of cell types across all cell clusters. The length of each bar indicates the Augur score, with longer bars indicating a stronger association with the Fibrosis+ phenotype. e Cellchat compares the total number of interactions and interaction strength of the inferred cell–cell communication networks between Fibrosis+ LM and Fibrosis− LM. f A heat map showing the contribution of signals (signaling pathways or LR pairs) to cell groups in terms of the overall signaling between Fibrosis+ LM and Fibrosis− LM, estimated by Cellchat. g The two-dimensional plots showing the incoming and outgoing interaction strengths for each of the cell types between Fibrosis+ LM and Fibrosis− LM. h The signaling changes of VCAN_eCAF from Fibrosis− LM to Fibrosis+ LM, estimated by Cellchat. i The significantly upregulated or downregulated LR pairs involved in ‘COLLAGEN’ signaling between VCAN_eCAF and other cells, such as MYH11_myoCAF, endothelial cells and MCs, estimated by iTALK. j, k The significantly upregulated or downregulated LR pairs in all signaling pathways between VCAN_eCAF and other cells, including T cells (j) and myeloid cells (k), estimated by iTALK.