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PRELP + CAFs interact and colocalize with immune cells in the tumor microenvironment. (a) Immunofluorescence staining in four groups showed spatial colocalization of PRELP (green) with aSMA (red), CD3 (red), CD20 (red) and <t>CD138</t> (red) in metastatic liver tumors, respectively. Magnified views of the boxed regions are shown on the right. Scale bars, 200 μm. (b) Bubble plot illustrating the incoming (vertical axis) and outgoing (horizontal axis) interaction strength of each cell subtype across all signaling pathways. Dot size represents the relative abundance of each cell type. (c) Predicted ligand-receptor (L–R) interactions between PRELP + CAFs and six immune cell subtypes in the APP-CD74 axis and the collagen-CD44 axis. Rows indicate specific L-R pairs, and columns represent immune cell subtypes. Dot color denotes the communication probability. (d) Predicted ligand-receptor (L–R) interactions of GALECTIN (top) and NECTIN (bottom) signaling pathways between PRELP + CAFs and TNK cell subtypes. Dot color represents the communication probability. (e) Hierarchical plots of the SEMA7A/(ITGB1+ITGA1) signaling network inferred by CellChat. Line thickness represents interaction strength and the color of line matches the signal sending cell. In the top panel, fibroblasts act as signal receivers, while in the bottom panel, myeloid cells receive the signals. (f) Bubble plot illustrating the incoming (vertical axis) and outgoing (horizontal axis) interaction strength of fibroblast and myeloid cell subtype in SEMA4 signaling pathways. Dot size represents the relative abundance of each cell type.
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Image Search Results


PRELP + CAFs interact and colocalize with immune cells in the tumor microenvironment. (a) Immunofluorescence staining in four groups showed spatial colocalization of PRELP (green) with aSMA (red), CD3 (red), CD20 (red) and CD138 (red) in metastatic liver tumors, respectively. Magnified views of the boxed regions are shown on the right. Scale bars, 200 μm. (b) Bubble plot illustrating the incoming (vertical axis) and outgoing (horizontal axis) interaction strength of each cell subtype across all signaling pathways. Dot size represents the relative abundance of each cell type. (c) Predicted ligand-receptor (L–R) interactions between PRELP + CAFs and six immune cell subtypes in the APP-CD74 axis and the collagen-CD44 axis. Rows indicate specific L-R pairs, and columns represent immune cell subtypes. Dot color denotes the communication probability. (d) Predicted ligand-receptor (L–R) interactions of GALECTIN (top) and NECTIN (bottom) signaling pathways between PRELP + CAFs and TNK cell subtypes. Dot color represents the communication probability. (e) Hierarchical plots of the SEMA7A/(ITGB1+ITGA1) signaling network inferred by CellChat. Line thickness represents interaction strength and the color of line matches the signal sending cell. In the top panel, fibroblasts act as signal receivers, while in the bottom panel, myeloid cells receive the signals. (f) Bubble plot illustrating the incoming (vertical axis) and outgoing (horizontal axis) interaction strength of fibroblast and myeloid cell subtype in SEMA4 signaling pathways. Dot size represents the relative abundance of each cell type.

Journal: Frontiers in Genetics

Article Title: Characterization of the phenotype and function of PRELP + fibroblast subtype in liver metastatic colorectal cancer

doi: 10.3389/fgene.2025.1615259

Figure Lengend Snippet: PRELP + CAFs interact and colocalize with immune cells in the tumor microenvironment. (a) Immunofluorescence staining in four groups showed spatial colocalization of PRELP (green) with aSMA (red), CD3 (red), CD20 (red) and CD138 (red) in metastatic liver tumors, respectively. Magnified views of the boxed regions are shown on the right. Scale bars, 200 μm. (b) Bubble plot illustrating the incoming (vertical axis) and outgoing (horizontal axis) interaction strength of each cell subtype across all signaling pathways. Dot size represents the relative abundance of each cell type. (c) Predicted ligand-receptor (L–R) interactions between PRELP + CAFs and six immune cell subtypes in the APP-CD74 axis and the collagen-CD44 axis. Rows indicate specific L-R pairs, and columns represent immune cell subtypes. Dot color denotes the communication probability. (d) Predicted ligand-receptor (L–R) interactions of GALECTIN (top) and NECTIN (bottom) signaling pathways between PRELP + CAFs and TNK cell subtypes. Dot color represents the communication probability. (e) Hierarchical plots of the SEMA7A/(ITGB1+ITGA1) signaling network inferred by CellChat. Line thickness represents interaction strength and the color of line matches the signal sending cell. In the top panel, fibroblasts act as signal receivers, while in the bottom panel, myeloid cells receive the signals. (f) Bubble plot illustrating the incoming (vertical axis) and outgoing (horizontal axis) interaction strength of fibroblast and myeloid cell subtype in SEMA4 signaling pathways. Dot size represents the relative abundance of each cell type.

Article Snippet: Rabbit anti-human PRELP (Abcam, ab229719, 1:100) was incubated overnight at 4 °C with mouse anti-human COL1A1 (CST, #6648, 1:200), mouse anti-human aSMA (Fluidgm, 3141017D, 1:200), mouse anti-human CD3 (Santa Cruz, sc-59010, 1:80), mouse anti-human CD138 (Santa Cruz, sc-12765, 1:100), and mouse anti-human CD20 (Servicebio, GB14030-50, 1:150) individually in separate reactions.

Techniques: Immunofluorescence, Staining, Protein-Protein interactions