mouse pca cell rm-1 Search Results


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Sangon Biotech rm 1 mouse prostate cancer cell line
Rm 1 Mouse Prostate Cancer Cell Line, supplied by Sangon Biotech, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ATCC rm 1 mouse prostate cancer cell lines
Rm 1 Mouse Prostate Cancer Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Procell Inc organoid culture 820 mouse prostate cancer rm 1 cells
Organoid Culture 820 Mouse Prostate Cancer Rm 1 Cells, supplied by Procell Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ATCC mouse prostate cancer cell line
Mouse Prostate Cancer Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ATCC mouse pca cell lines
Suppressing stromal MAOA activity in vivo can effectively inhibit the proliferation of prostate cancer xenografts by potentiating the immune-killing function of CD8 + T cells. ( A ) Schematic diagram of the construction of a subcutaneous tumor graft model in C57BL/6J mice and the drug administration strategy. ( B ) Tumor growth curves of mice in different treatment groups. ( C ) Representative images and quantification results of KI-67 + and Tunel + in mice from different treatment groups, scale bars, 50 µm. ( D ) Representative images and quantification results of CD8 + T cells in different treatment groups of mice, scale bars, 50 µm. ( E ) FACS analysis of the proportion of CD8 + CD45 + T cells in tumor tissues from different treatment groups. ( F ) ELISA experiments to detect the content of IFN-γ in tumor tissues from different treatment groups. ( G ) Strategy for the construction of double humanized <t>PCa</t> <t>mouse</t> model and administration. ( H ) The tumor growth curves of mice in the NC group and the sh-MAOA group. ( I ) Representative images and quantification results of KI-67 + and Tunnel + for mice in the NC group and sh-MAOA group, scale bars, 50 µm. ( J ) Representative images and quantification results of CD8 + T cells in the NC group and sh-MAOA group of mice. Scale bars, 50 µm. ( K ) FACS analysis of the proportion of CD8 + CD45 + T cells in tumor tissues from NC group and sh-MAOA group. ( L ) ELISA experiments to detect the content of IFN-γ in tumor tissues from NC group and sh-MAOA group. Clo, chlorgyline; Con, control; DAPI, 4',6-Diamidino-2-Phenylindole; FACS, fluorescence-activated <t>cell</t> sorting; M-PrSC, mouse primary stromal cells; NC, negative control; PBMC, peripheral blood mononuclear cell; PCa, prostate cancer; Phe, phenelzine; sh-MAOA, short hairpin RNA targeting monoamine oxidase A.
Mouse Pca Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mouse+pca+cell+rm-1/TRAMP-C1/pmc11931948-34-8-29
Average 96 stars, based on 1 article reviews
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86
Procell Inc mouse prostate cancer cells
Suppressing stromal MAOA activity in vivo can effectively inhibit the proliferation of prostate cancer xenografts by potentiating the immune-killing function of CD8 + T cells. ( A ) Schematic diagram of the construction of a subcutaneous tumor graft model in C57BL/6J mice and the drug administration strategy. ( B ) Tumor growth curves of mice in different treatment groups. ( C ) Representative images and quantification results of KI-67 + and Tunel + in mice from different treatment groups, scale bars, 50 µm. ( D ) Representative images and quantification results of CD8 + T cells in different treatment groups of mice, scale bars, 50 µm. ( E ) FACS analysis of the proportion of CD8 + CD45 + T cells in tumor tissues from different treatment groups. ( F ) ELISA experiments to detect the content of IFN-γ in tumor tissues from different treatment groups. ( G ) Strategy for the construction of double humanized <t>PCa</t> <t>mouse</t> model and administration. ( H ) The tumor growth curves of mice in the NC group and the sh-MAOA group. ( I ) Representative images and quantification results of KI-67 + and Tunnel + for mice in the NC group and sh-MAOA group, scale bars, 50 µm. ( J ) Representative images and quantification results of CD8 + T cells in the NC group and sh-MAOA group of mice. Scale bars, 50 µm. ( K ) FACS analysis of the proportion of CD8 + CD45 + T cells in tumor tissues from NC group and sh-MAOA group. ( L ) ELISA experiments to detect the content of IFN-γ in tumor tissues from NC group and sh-MAOA group. Clo, chlorgyline; Con, control; DAPI, 4',6-Diamidino-2-Phenylindole; FACS, fluorescence-activated <t>cell</t> sorting; M-PrSC, mouse primary stromal cells; NC, negative control; PBMC, peripheral blood mononuclear cell; PCa, prostate cancer; Phe, phenelzine; sh-MAOA, short hairpin RNA targeting monoamine oxidase A.
Mouse Prostate Cancer Cells, supplied by Procell Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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93
MedChemExpress anti erbb3 monoclonal antibody
Cell–cell communication analysis reveals B cell-specific interaction rewiring in <t>ERBB3-high</t> tumors. Sample-wise composition of high vs. low ERBB3-expressing groups in an independent HNSCC scRNA-seq dataset.(B) Total number and average strength of inferred interactions across groups. (C) CellChat plots showing differential epithelial cell interactions; B cells exhibited the most dramatic rewiring. Red arrows indicate enhanced ligand–receptor interactions in the ERBB3-high group, whereas blue arrows indicate decreased interactions compared to the ERBB3-low group.(D–E) UMAP projection and further subclustering of B cells.(F) Bubble plot showing differential ligand–receptor interactions involving TNFRSF13B, IL4R, and IGHG between ERBB3-high and ERBB3-low groups. Each dot represents a ligand–receptor pair, where dot size indicates communication strength (interaction probability) and color intensity reflects statistical significance. Notably, signaling via TNFRSF13B, IL4R, and IGHG shows reduced interaction strength and significance in the ERBB3-high group. (G) Cell-type proportions in each group.(H) Pathway-specific interaction plots highlighting TNFRSF13B + B cell axes.(I) Heatmaps of differential interaction numbers and strengths.(J) Relative information flow of signaling pathways.(K) Dot plot of significant differential ligand–receptor pairs with p-values and communication probability
Anti Erbb3 Monoclonal Antibody, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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China Center for Type Culture Collection mouse prostate cancer cell line rm-1
Cell–cell communication analysis reveals B cell-specific interaction rewiring in <t>ERBB3-high</t> tumors. Sample-wise composition of high vs. low ERBB3-expressing groups in an independent HNSCC scRNA-seq dataset.(B) Total number and average strength of inferred interactions across groups. (C) CellChat plots showing differential epithelial cell interactions; B cells exhibited the most dramatic rewiring. Red arrows indicate enhanced ligand–receptor interactions in the ERBB3-high group, whereas blue arrows indicate decreased interactions compared to the ERBB3-low group.(D–E) UMAP projection and further subclustering of B cells.(F) Bubble plot showing differential ligand–receptor interactions involving TNFRSF13B, IL4R, and IGHG between ERBB3-high and ERBB3-low groups. Each dot represents a ligand–receptor pair, where dot size indicates communication strength (interaction probability) and color intensity reflects statistical significance. Notably, signaling via TNFRSF13B, IL4R, and IGHG shows reduced interaction strength and significance in the ERBB3-high group. (G) Cell-type proportions in each group.(H) Pathway-specific interaction plots highlighting TNFRSF13B + B cell axes.(I) Heatmaps of differential interaction numbers and strengths.(J) Relative information flow of signaling pathways.(K) Dot plot of significant differential ligand–receptor pairs with p-values and communication probability
Mouse Prostate Cancer Cell Line Rm 1, supplied by China Center for Type Culture Collection, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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iCell Bioscience Inc mouse prostate cancer cells rm-1
Cell–cell communication analysis reveals B cell-specific interaction rewiring in <t>ERBB3-high</t> tumors. Sample-wise composition of high vs. low ERBB3-expressing groups in an independent HNSCC scRNA-seq dataset.(B) Total number and average strength of inferred interactions across groups. (C) CellChat plots showing differential epithelial cell interactions; B cells exhibited the most dramatic rewiring. Red arrows indicate enhanced ligand–receptor interactions in the ERBB3-high group, whereas blue arrows indicate decreased interactions compared to the ERBB3-low group.(D–E) UMAP projection and further subclustering of B cells.(F) Bubble plot showing differential ligand–receptor interactions involving TNFRSF13B, IL4R, and IGHG between ERBB3-high and ERBB3-low groups. Each dot represents a ligand–receptor pair, where dot size indicates communication strength (interaction probability) and color intensity reflects statistical significance. Notably, signaling via TNFRSF13B, IL4R, and IGHG shows reduced interaction strength and significance in the ERBB3-high group. (G) Cell-type proportions in each group.(H) Pathway-specific interaction plots highlighting TNFRSF13B + B cell axes.(I) Heatmaps of differential interaction numbers and strengths.(J) Relative information flow of signaling pathways.(K) Dot plot of significant differential ligand–receptor pairs with p-values and communication probability
Mouse Prostate Cancer Cells Rm 1, supplied by iCell Bioscience Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mouse+pca+cell+rm-1/mouse+prostate+cancer+cells+rm+1/pmc08114913-35-0-16
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ATCC mouse rm 1 cell line
Cell–cell communication analysis reveals B cell-specific interaction rewiring in <t>ERBB3-high</t> tumors. Sample-wise composition of high vs. low ERBB3-expressing groups in an independent HNSCC scRNA-seq dataset.(B) Total number and average strength of inferred interactions across groups. (C) CellChat plots showing differential epithelial cell interactions; B cells exhibited the most dramatic rewiring. Red arrows indicate enhanced ligand–receptor interactions in the ERBB3-high group, whereas blue arrows indicate decreased interactions compared to the ERBB3-low group.(D–E) UMAP projection and further subclustering of B cells.(F) Bubble plot showing differential ligand–receptor interactions involving TNFRSF13B, IL4R, and IGHG between ERBB3-high and ERBB3-low groups. Each dot represents a ligand–receptor pair, where dot size indicates communication strength (interaction probability) and color intensity reflects statistical significance. Notably, signaling via TNFRSF13B, IL4R, and IGHG shows reduced interaction strength and significance in the ERBB3-high group. (G) Cell-type proportions in each group.(H) Pathway-specific interaction plots highlighting TNFRSF13B + B cell axes.(I) Heatmaps of differential interaction numbers and strengths.(J) Relative information flow of signaling pathways.(K) Dot plot of significant differential ligand–receptor pairs with p-values and communication probability
Mouse Rm 1 Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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National Centre for Cell Science model tumor induced by rm-1 cells
Cell–cell communication analysis reveals B cell-specific interaction rewiring in <t>ERBB3-high</t> tumors. Sample-wise composition of high vs. low ERBB3-expressing groups in an independent HNSCC scRNA-seq dataset.(B) Total number and average strength of inferred interactions across groups. (C) CellChat plots showing differential epithelial cell interactions; B cells exhibited the most dramatic rewiring. Red arrows indicate enhanced ligand–receptor interactions in the ERBB3-high group, whereas blue arrows indicate decreased interactions compared to the ERBB3-low group.(D–E) UMAP projection and further subclustering of B cells.(F) Bubble plot showing differential ligand–receptor interactions involving TNFRSF13B, IL4R, and IGHG between ERBB3-high and ERBB3-low groups. Each dot represents a ligand–receptor pair, where dot size indicates communication strength (interaction probability) and color intensity reflects statistical significance. Notably, signaling via TNFRSF13B, IL4R, and IGHG shows reduced interaction strength and significance in the ERBB3-high group. (G) Cell-type proportions in each group.(H) Pathway-specific interaction plots highlighting TNFRSF13B + B cell axes.(I) Heatmaps of differential interaction numbers and strengths.(J) Relative information flow of signaling pathways.(K) Dot plot of significant differential ligand–receptor pairs with p-values and communication probability
Model Tumor Induced By Rm 1 Cells, supplied by National Centre for Cell Science, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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model tumor induced by rm-1 cells - by Bioz Stars, 2026-10
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99
CancerTools Org mb49
Cell–cell communication analysis reveals B cell-specific interaction rewiring in <t>ERBB3-high</t> tumors. Sample-wise composition of high vs. low ERBB3-expressing groups in an independent HNSCC scRNA-seq dataset.(B) Total number and average strength of inferred interactions across groups. (C) CellChat plots showing differential epithelial cell interactions; B cells exhibited the most dramatic rewiring. Red arrows indicate enhanced ligand–receptor interactions in the ERBB3-high group, whereas blue arrows indicate decreased interactions compared to the ERBB3-low group.(D–E) UMAP projection and further subclustering of B cells.(F) Bubble plot showing differential ligand–receptor interactions involving TNFRSF13B, IL4R, and IGHG between ERBB3-high and ERBB3-low groups. Each dot represents a ligand–receptor pair, where dot size indicates communication strength (interaction probability) and color intensity reflects statistical significance. Notably, signaling via TNFRSF13B, IL4R, and IGHG shows reduced interaction strength and significance in the ERBB3-high group. (G) Cell-type proportions in each group.(H) Pathway-specific interaction plots highlighting TNFRSF13B + B cell axes.(I) Heatmaps of differential interaction numbers and strengths.(J) Relative information flow of signaling pathways.(K) Dot plot of significant differential ligand–receptor pairs with p-values and communication probability
Mb49, supplied by CancerTools Org, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Suppressing stromal MAOA activity in vivo can effectively inhibit the proliferation of prostate cancer xenografts by potentiating the immune-killing function of CD8 + T cells. ( A ) Schematic diagram of the construction of a subcutaneous tumor graft model in C57BL/6J mice and the drug administration strategy. ( B ) Tumor growth curves of mice in different treatment groups. ( C ) Representative images and quantification results of KI-67 + and Tunel + in mice from different treatment groups, scale bars, 50 µm. ( D ) Representative images and quantification results of CD8 + T cells in different treatment groups of mice, scale bars, 50 µm. ( E ) FACS analysis of the proportion of CD8 + CD45 + T cells in tumor tissues from different treatment groups. ( F ) ELISA experiments to detect the content of IFN-γ in tumor tissues from different treatment groups. ( G ) Strategy for the construction of double humanized PCa mouse model and administration. ( H ) The tumor growth curves of mice in the NC group and the sh-MAOA group. ( I ) Representative images and quantification results of KI-67 + and Tunnel + for mice in the NC group and sh-MAOA group, scale bars, 50 µm. ( J ) Representative images and quantification results of CD8 + T cells in the NC group and sh-MAOA group of mice. Scale bars, 50 µm. ( K ) FACS analysis of the proportion of CD8 + CD45 + T cells in tumor tissues from NC group and sh-MAOA group. ( L ) ELISA experiments to detect the content of IFN-γ in tumor tissues from NC group and sh-MAOA group. Clo, chlorgyline; Con, control; DAPI, 4',6-Diamidino-2-Phenylindole; FACS, fluorescence-activated cell sorting; M-PrSC, mouse primary stromal cells; NC, negative control; PBMC, peripheral blood mononuclear cell; PCa, prostate cancer; Phe, phenelzine; sh-MAOA, short hairpin RNA targeting monoamine oxidase A.

Journal: Journal for Immunotherapy of Cancer

Article Title: Inhibition of stromal MAOA leading activation of WNT5A enhance prostate cancer immunotherapy by involving the transition of cancer-associated fibroblasts

doi: 10.1136/jitc-2024-010555

Figure Lengend Snippet: Suppressing stromal MAOA activity in vivo can effectively inhibit the proliferation of prostate cancer xenografts by potentiating the immune-killing function of CD8 + T cells. ( A ) Schematic diagram of the construction of a subcutaneous tumor graft model in C57BL/6J mice and the drug administration strategy. ( B ) Tumor growth curves of mice in different treatment groups. ( C ) Representative images and quantification results of KI-67 + and Tunel + in mice from different treatment groups, scale bars, 50 µm. ( D ) Representative images and quantification results of CD8 + T cells in different treatment groups of mice, scale bars, 50 µm. ( E ) FACS analysis of the proportion of CD8 + CD45 + T cells in tumor tissues from different treatment groups. ( F ) ELISA experiments to detect the content of IFN-γ in tumor tissues from different treatment groups. ( G ) Strategy for the construction of double humanized PCa mouse model and administration. ( H ) The tumor growth curves of mice in the NC group and the sh-MAOA group. ( I ) Representative images and quantification results of KI-67 + and Tunnel + for mice in the NC group and sh-MAOA group, scale bars, 50 µm. ( J ) Representative images and quantification results of CD8 + T cells in the NC group and sh-MAOA group of mice. Scale bars, 50 µm. ( K ) FACS analysis of the proportion of CD8 + CD45 + T cells in tumor tissues from NC group and sh-MAOA group. ( L ) ELISA experiments to detect the content of IFN-γ in tumor tissues from NC group and sh-MAOA group. Clo, chlorgyline; Con, control; DAPI, 4',6-Diamidino-2-Phenylindole; FACS, fluorescence-activated cell sorting; M-PrSC, mouse primary stromal cells; NC, negative control; PBMC, peripheral blood mononuclear cell; PCa, prostate cancer; Phe, phenelzine; sh-MAOA, short hairpin RNA targeting monoamine oxidase A.

Article Snippet: Human PCa cell lines (PC3, DU145, C42, 22RV1), mouse PCa cell lines (RM-1, Tramp-C1), Human prostate stromal myofibroblast (WPMY-1) and Human leukemia cell line (JURKAT) were obtained from the American Type Culture Collection (Manassas, Virginia, USA) and cultured in Roswell Park Memorial Institute 1640 and Dulbecco’s Modified Eagle’s Medium supplemented with 10% fetal bovine serum (Gibco).

Techniques: Activity Assay, In Vivo, TUNEL Assay, Enzyme-linked Immunosorbent Assay, Control, Fluorescence, FACS, Negative Control, shRNA

Inhibition of stromal MAOA sensitizes prostate cancer cells to the therapeutic effects of immune checkpoint inhibitors. ( A ) Strategy for the construction of subcutaneous tumor xenograft model in C57BL/6J mouse model and administration. ( B ) Tumor growth curves of mice in different treatment groups. ( C ) The expression of WNT5A, the proportion of CD8 + T cells, and the content of IFN-γ in different treatment groups of mice tumor tissues. ( D ) Strategy for the construction of double humanized PCa mouse model and administration. ( E ) Tumor growth curves of mice in different treatment groups. ( F ) The expression of WNT5A, the proportion of CD8 + T cells, and the content of IFN-γ in different treatment groups of mice tumor tissues. ( G ) A schematic diagram of the mechanism by which inhibiting MAOA in tumor-associated fibroblasts exerts antitumor effects. Availability of data and material: the datasets generated during and/or analyzed during the current study are available from the corresponding author on reasonable request. CAF, cancer-associated fibroblast; Clo, chlorgyline; Con, Control; MAOA, monoamine oxidase A; M-PrSC, mouse primary stromal cells; ns, not significant; PBMC, peripheral blood mononuclear cell; PCa, prostate cancer; PD-1, programmed cell death protein-1; ROS, Reactive Oxygen Species; sh-MAOA, short hairpin RNA targeting MAOA; WT, Wild Type.

Journal: Journal for Immunotherapy of Cancer

Article Title: Inhibition of stromal MAOA leading activation of WNT5A enhance prostate cancer immunotherapy by involving the transition of cancer-associated fibroblasts

doi: 10.1136/jitc-2024-010555

Figure Lengend Snippet: Inhibition of stromal MAOA sensitizes prostate cancer cells to the therapeutic effects of immune checkpoint inhibitors. ( A ) Strategy for the construction of subcutaneous tumor xenograft model in C57BL/6J mouse model and administration. ( B ) Tumor growth curves of mice in different treatment groups. ( C ) The expression of WNT5A, the proportion of CD8 + T cells, and the content of IFN-γ in different treatment groups of mice tumor tissues. ( D ) Strategy for the construction of double humanized PCa mouse model and administration. ( E ) Tumor growth curves of mice in different treatment groups. ( F ) The expression of WNT5A, the proportion of CD8 + T cells, and the content of IFN-γ in different treatment groups of mice tumor tissues. ( G ) A schematic diagram of the mechanism by which inhibiting MAOA in tumor-associated fibroblasts exerts antitumor effects. Availability of data and material: the datasets generated during and/or analyzed during the current study are available from the corresponding author on reasonable request. CAF, cancer-associated fibroblast; Clo, chlorgyline; Con, Control; MAOA, monoamine oxidase A; M-PrSC, mouse primary stromal cells; ns, not significant; PBMC, peripheral blood mononuclear cell; PCa, prostate cancer; PD-1, programmed cell death protein-1; ROS, Reactive Oxygen Species; sh-MAOA, short hairpin RNA targeting MAOA; WT, Wild Type.

Article Snippet: Human PCa cell lines (PC3, DU145, C42, 22RV1), mouse PCa cell lines (RM-1, Tramp-C1), Human prostate stromal myofibroblast (WPMY-1) and Human leukemia cell line (JURKAT) were obtained from the American Type Culture Collection (Manassas, Virginia, USA) and cultured in Roswell Park Memorial Institute 1640 and Dulbecco’s Modified Eagle’s Medium supplemented with 10% fetal bovine serum (Gibco).

Techniques: Inhibition, Expressing, Generated, Control, shRNA

Cell–cell communication analysis reveals B cell-specific interaction rewiring in ERBB3-high tumors. Sample-wise composition of high vs. low ERBB3-expressing groups in an independent HNSCC scRNA-seq dataset.(B) Total number and average strength of inferred interactions across groups. (C) CellChat plots showing differential epithelial cell interactions; B cells exhibited the most dramatic rewiring. Red arrows indicate enhanced ligand–receptor interactions in the ERBB3-high group, whereas blue arrows indicate decreased interactions compared to the ERBB3-low group.(D–E) UMAP projection and further subclustering of B cells.(F) Bubble plot showing differential ligand–receptor interactions involving TNFRSF13B, IL4R, and IGHG between ERBB3-high and ERBB3-low groups. Each dot represents a ligand–receptor pair, where dot size indicates communication strength (interaction probability) and color intensity reflects statistical significance. Notably, signaling via TNFRSF13B, IL4R, and IGHG shows reduced interaction strength and significance in the ERBB3-high group. (G) Cell-type proportions in each group.(H) Pathway-specific interaction plots highlighting TNFRSF13B + B cell axes.(I) Heatmaps of differential interaction numbers and strengths.(J) Relative information flow of signaling pathways.(K) Dot plot of significant differential ligand–receptor pairs with p-values and communication probability

Journal: Discover Oncology

Article Title: Single-cell profiling of ERBB family receptors identifies ERBB3 as a key regulator in head and neck squamous cell carcinoma progression

doi: 10.1007/s12672-025-03681-y

Figure Lengend Snippet: Cell–cell communication analysis reveals B cell-specific interaction rewiring in ERBB3-high tumors. Sample-wise composition of high vs. low ERBB3-expressing groups in an independent HNSCC scRNA-seq dataset.(B) Total number and average strength of inferred interactions across groups. (C) CellChat plots showing differential epithelial cell interactions; B cells exhibited the most dramatic rewiring. Red arrows indicate enhanced ligand–receptor interactions in the ERBB3-high group, whereas blue arrows indicate decreased interactions compared to the ERBB3-low group.(D–E) UMAP projection and further subclustering of B cells.(F) Bubble plot showing differential ligand–receptor interactions involving TNFRSF13B, IL4R, and IGHG between ERBB3-high and ERBB3-low groups. Each dot represents a ligand–receptor pair, where dot size indicates communication strength (interaction probability) and color intensity reflects statistical significance. Notably, signaling via TNFRSF13B, IL4R, and IGHG shows reduced interaction strength and significance in the ERBB3-high group. (G) Cell-type proportions in each group.(H) Pathway-specific interaction plots highlighting TNFRSF13B + B cell axes.(I) Heatmaps of differential interaction numbers and strengths.(J) Relative information flow of signaling pathways.(K) Dot plot of significant differential ligand–receptor pairs with p-values and communication probability

Article Snippet: Mice in the treatment group received intraperitoneal injections of anti-ERBB3 monoclonal antibody (MP-RM-1, MCE) at a dose of 10 mg/kg, twice per week for three consecutive weeks.

Techniques: Expressing, Protein-Protein interactions

Prognostic modeling based on ERBB pathway activity and tumor microenvironment features. (A) Risk score distribution, survival status, and heatmap of ERBB family gene expression across TCGA patients.(B) Kaplan–Meier overall survival curves comparing high- and low-risk groups based on LASSO-derived ERBB prognostic signature.(C) Expression of ERBB3, EGFR, ERBB2, and ERBB4 between risk groups.(D) Time-dependent ROC curves showing prognostic performance of the risk model. The AUCs were 0.68 (1 year), 0.71 (3 years), and 0.74 (5 years).(E–H) Violin plots comparing ESTIMATE score, tumor purity, stromal score, and immune score between high- and low-risk groups.(I) Bar plot showing CIBERSORTx deconvolution of immune infiltration across groups.(J–K) Validation of risk model in GEO dataset, including survival curve and ROC analysis

Journal: Discover Oncology

Article Title: Single-cell profiling of ERBB family receptors identifies ERBB3 as a key regulator in head and neck squamous cell carcinoma progression

doi: 10.1007/s12672-025-03681-y

Figure Lengend Snippet: Prognostic modeling based on ERBB pathway activity and tumor microenvironment features. (A) Risk score distribution, survival status, and heatmap of ERBB family gene expression across TCGA patients.(B) Kaplan–Meier overall survival curves comparing high- and low-risk groups based on LASSO-derived ERBB prognostic signature.(C) Expression of ERBB3, EGFR, ERBB2, and ERBB4 between risk groups.(D) Time-dependent ROC curves showing prognostic performance of the risk model. The AUCs were 0.68 (1 year), 0.71 (3 years), and 0.74 (5 years).(E–H) Violin plots comparing ESTIMATE score, tumor purity, stromal score, and immune score between high- and low-risk groups.(I) Bar plot showing CIBERSORTx deconvolution of immune infiltration across groups.(J–K) Validation of risk model in GEO dataset, including survival curve and ROC analysis

Article Snippet: Mice in the treatment group received intraperitoneal injections of anti-ERBB3 monoclonal antibody (MP-RM-1, MCE) at a dose of 10 mg/kg, twice per week for three consecutive weeks.

Techniques: Activity Assay, Gene Expression, Derivative Assay, Expressing, Biomarker Discovery

Prognostic value and clinical correlation of ERBB family members in HNSCC. (A–D) Kaplan–Meier curves for EGFR, ERBB2, ERBB3, and ERBB4; ERBB3-high patients show better overall survival ( p = 0.028).(E) Boxplot comparing ERBB3 expression in normal ( n = 44) and tumor tissues ( n = 520) from TCGA.(F) ERBB3 expression across pathological grades; higher expression observed in grade 4 tumors ( n = 7)

Journal: Discover Oncology

Article Title: Single-cell profiling of ERBB family receptors identifies ERBB3 as a key regulator in head and neck squamous cell carcinoma progression

doi: 10.1007/s12672-025-03681-y

Figure Lengend Snippet: Prognostic value and clinical correlation of ERBB family members in HNSCC. (A–D) Kaplan–Meier curves for EGFR, ERBB2, ERBB3, and ERBB4; ERBB3-high patients show better overall survival ( p = 0.028).(E) Boxplot comparing ERBB3 expression in normal ( n = 44) and tumor tissues ( n = 520) from TCGA.(F) ERBB3 expression across pathological grades; higher expression observed in grade 4 tumors ( n = 7)

Article Snippet: Mice in the treatment group received intraperitoneal injections of anti-ERBB3 monoclonal antibody (MP-RM-1, MCE) at a dose of 10 mg/kg, twice per week for three consecutive weeks.

Techniques: Expressing

ERBB3 knockdown impairs proliferation, colony formation, migration, and invasion in SCC9 cells. (A) ERBB3 protein levels across HNSCC cell lines based on DepMap portal.(B–C) Validation of ERBB3 knockdown by lentiviral shRNA via western blot and qRT-PCR.(D) Cell proliferation measured by CCK-8 assays over four days.(E–F) Representative images and quantification of colony formation assays.(G–H) Representative transwell migration assay and quantification.(I–J) Transwell invasion assay and quantification. Data are presented as mean ± SD; * p < 0.05, ** p < 0.01, *** p < 0.001

Journal: Discover Oncology

Article Title: Single-cell profiling of ERBB family receptors identifies ERBB3 as a key regulator in head and neck squamous cell carcinoma progression

doi: 10.1007/s12672-025-03681-y

Figure Lengend Snippet: ERBB3 knockdown impairs proliferation, colony formation, migration, and invasion in SCC9 cells. (A) ERBB3 protein levels across HNSCC cell lines based on DepMap portal.(B–C) Validation of ERBB3 knockdown by lentiviral shRNA via western blot and qRT-PCR.(D) Cell proliferation measured by CCK-8 assays over four days.(E–F) Representative images and quantification of colony formation assays.(G–H) Representative transwell migration assay and quantification.(I–J) Transwell invasion assay and quantification. Data are presented as mean ± SD; * p < 0.05, ** p < 0.01, *** p < 0.001

Article Snippet: Mice in the treatment group received intraperitoneal injections of anti-ERBB3 monoclonal antibody (MP-RM-1, MCE) at a dose of 10 mg/kg, twice per week for three consecutive weeks.

Techniques: Knockdown, Migration, Biomarker Discovery, shRNA, Western Blot, Quantitative RT-PCR, CCK-8 Assay, Transwell Migration Assay, Transwell Invasion Assay

ERBB3 inhibition modulates immunosuppressive B cell phenotypes in vivo.、(A) Volcano plot showing differentially expressed genes between Scissor-high and Scissor-low tumor cell subsets.(B) KEGG enrichment showing suppression of antigen presentation pathways in ERBB3-high B cells.(C) Violin plot of CCDC50 expression in CD45⁺MS4A1⁺ B cells stratified by ERBB3 status.(D) UMAP projection of CCDC50 expression in single-cell data.(E) Flow cytometry showing reduced TNFRSF13B⁺CCDC50⁺ B cells upon ERBB3 inhibitor treatment.(F) Flow cytometry of MHC-II⁺ B cells showing enhanced antigen presentation following ERBB3 inhibition ( n = 3 mice per group). Data are shown as mean ± SEM. Statistical significance was determined using two-tailed unpaired Student’s t-test. * p < 0.05; ** p < 0.01, *** p < 0.001

Journal: Discover Oncology

Article Title: Single-cell profiling of ERBB family receptors identifies ERBB3 as a key regulator in head and neck squamous cell carcinoma progression

doi: 10.1007/s12672-025-03681-y

Figure Lengend Snippet: ERBB3 inhibition modulates immunosuppressive B cell phenotypes in vivo.、(A) Volcano plot showing differentially expressed genes between Scissor-high and Scissor-low tumor cell subsets.(B) KEGG enrichment showing suppression of antigen presentation pathways in ERBB3-high B cells.(C) Violin plot of CCDC50 expression in CD45⁺MS4A1⁺ B cells stratified by ERBB3 status.(D) UMAP projection of CCDC50 expression in single-cell data.(E) Flow cytometry showing reduced TNFRSF13B⁺CCDC50⁺ B cells upon ERBB3 inhibitor treatment.(F) Flow cytometry of MHC-II⁺ B cells showing enhanced antigen presentation following ERBB3 inhibition ( n = 3 mice per group). Data are shown as mean ± SEM. Statistical significance was determined using two-tailed unpaired Student’s t-test. * p < 0.05; ** p < 0.01, *** p < 0.001

Article Snippet: Mice in the treatment group received intraperitoneal injections of anti-ERBB3 monoclonal antibody (MP-RM-1, MCE) at a dose of 10 mg/kg, twice per week for three consecutive weeks.

Techniques: Inhibition, In Vivo, Immunopeptidomics, Expressing, Flow Cytometry, Two Tailed Test