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Break-down comparison of Ω 1 (blue), Ω 2 (orange), and Ω 3 (gray) among methods for <t>EMP1</t> (upper left), EMP2 (upper right), STD1 (lower left), and STD2 (lower right).
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Establishment and validation of the E3-related prognostic signature. ( A ) Multivariate Cox coefficients for seven genes ( <t>EMP1</t> , CLSTN2 , SERPINB2 , PTGER3 , SULT1C2 , XDH , and SLC26A8 ) in the prognostic signature. ( B ) Risk score distribution among BLCA patients, sorted from lowest to highest. ( C ) Survival status categorized by Riskscore for each BLCA patient. ( D ) Sankey diagram correlating clusters, risk groups, and BLCA survival status. ( E ) Heatmap displaying expression levels of seven genes in different Riskscore groups. ( F ) Kaplan-Meier analysis comparing overall survival between high and low Riskscore groups in BLCA ( P < 0.0001). ( G ) Receiver Operating Characteristic (ROC) curves depicting Riskscore signature’s predictive performance for 1, 3, and 5-year overall survival in BLCA. (H-K) Kaplan-Meier analysis and time-dependent ROC curves in two external validation sets: GSE32548 and GSE32894
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Fig. 1 The TME infiltration landscape, expression signature, and prognosis of <t>EMP1</t> in breast cancer. A Schematic diagram of the correlation analysis between EMP1 expression and different tumor microenvironments (TMEs) with regard to cell infiltration. B Correlation between EMP1 expression and the infiltration of different TME-related cell types. C The TME cell-infiltrating landscape in BC patients with high or low EMP1 expression. D Gene expression correlation analysis between EMP1 and the classic CAF biomarkers in the TCGA_BRCA cohort. E Expression analysis of EMP1 in different PAM50 subtypes of BC. F, G BC patients with relatively high EMP1 expression possessed shorter overall survival and disease-free survival times. H, I Overall survival and disease-free survival of patients with BC. Higher EMP1 expression in patients with BC did not correlate with overall or disease-free survival. J Survival analysis of EMP1 for each PAM50 subtype in patients with BC.
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Image Search Results


Break-down comparison of Ω 1 (blue), Ω 2 (orange), and Ω 3 (gray) among methods for EMP1 (upper left), EMP2 (upper right), STD1 (lower left), and STD2 (lower right).

Journal: PeerJ Computer Science

Article Title: Unbiased machine learning-assisted approach for conditional discretization of human performances

doi: 10.7717/peerj-cs.2804

Figure Lengend Snippet: Break-down comparison of Ω 1 (blue), Ω 2 (orange), and Ω 3 (gray) among methods for EMP1 (upper left), EMP2 (upper right), STD1 (lower left), and STD2 (lower right).

Article Snippet: The EMP1 dataset is available at Kaggle: https://www.kaggle.com/datasets/muhammadimran112233/employees-evaluation-for-promotion .

Techniques: Comparison

Establishment and validation of the E3-related prognostic signature. ( A ) Multivariate Cox coefficients for seven genes ( EMP1 , CLSTN2 , SERPINB2 , PTGER3 , SULT1C2 , XDH , and SLC26A8 ) in the prognostic signature. ( B ) Risk score distribution among BLCA patients, sorted from lowest to highest. ( C ) Survival status categorized by Riskscore for each BLCA patient. ( D ) Sankey diagram correlating clusters, risk groups, and BLCA survival status. ( E ) Heatmap displaying expression levels of seven genes in different Riskscore groups. ( F ) Kaplan-Meier analysis comparing overall survival between high and low Riskscore groups in BLCA ( P < 0.0001). ( G ) Receiver Operating Characteristic (ROC) curves depicting Riskscore signature’s predictive performance for 1, 3, and 5-year overall survival in BLCA. (H-K) Kaplan-Meier analysis and time-dependent ROC curves in two external validation sets: GSE32548 and GSE32894

Journal: Cancer Cell International

Article Title: Identification of E3 ubiquitin ligase-based molecular subtypes and prognostic signature regarding prognosis and immune landscape in bladder cancer

doi: 10.1186/s12935-025-03703-3

Figure Lengend Snippet: Establishment and validation of the E3-related prognostic signature. ( A ) Multivariate Cox coefficients for seven genes ( EMP1 , CLSTN2 , SERPINB2 , PTGER3 , SULT1C2 , XDH , and SLC26A8 ) in the prognostic signature. ( B ) Risk score distribution among BLCA patients, sorted from lowest to highest. ( C ) Survival status categorized by Riskscore for each BLCA patient. ( D ) Sankey diagram correlating clusters, risk groups, and BLCA survival status. ( E ) Heatmap displaying expression levels of seven genes in different Riskscore groups. ( F ) Kaplan-Meier analysis comparing overall survival between high and low Riskscore groups in BLCA ( P < 0.0001). ( G ) Receiver Operating Characteristic (ROC) curves depicting Riskscore signature’s predictive performance for 1, 3, and 5-year overall survival in BLCA. (H-K) Kaplan-Meier analysis and time-dependent ROC curves in two external validation sets: GSE32548 and GSE32894

Article Snippet: Primary antibodies against EMP1 (1:1000, Proteintech), SLC26A8 (1:1000, ABclonal) and β-actin (1:5000, Proteintech) were used.

Techniques: Expressing

High- and low-risk group patients differ in drug sensitivity. ( A ) Bubble plot showing the relationship between IC50 of drugs, risk score, and model genes. ( B - C ) Boxplot showing the comparison of IC50 of Oxaliplatin between high/low-risk groups, and scatter plot showing the correlation between the IC50 of drug and risk score. ( D - E ) Boxplot showing the comparison of IC50 of Oxaliplatin between low/high expression of EMP1, and scatter plot showing the correlation between the IC50 of drug and expression of EMP1. ( F ) Relative RNA levels of EMP1 in UMUC14, T24 and 5637 cells. ( G ) The protein levels of EMP1 were detected by Western blotting. ( H - J ) UMUC14, T24 and 5637 cells were treated with con siRNA, EMP1 siRNA, oxaliplatin (OXP, 50 µg/ml), or EMP1 siRNA + OXP. Cell viability was measured by CCK8 assay

Journal: Cancer Cell International

Article Title: Identification of E3 ubiquitin ligase-based molecular subtypes and prognostic signature regarding prognosis and immune landscape in bladder cancer

doi: 10.1186/s12935-025-03703-3

Figure Lengend Snippet: High- and low-risk group patients differ in drug sensitivity. ( A ) Bubble plot showing the relationship between IC50 of drugs, risk score, and model genes. ( B - C ) Boxplot showing the comparison of IC50 of Oxaliplatin between high/low-risk groups, and scatter plot showing the correlation between the IC50 of drug and risk score. ( D - E ) Boxplot showing the comparison of IC50 of Oxaliplatin between low/high expression of EMP1, and scatter plot showing the correlation between the IC50 of drug and expression of EMP1. ( F ) Relative RNA levels of EMP1 in UMUC14, T24 and 5637 cells. ( G ) The protein levels of EMP1 were detected by Western blotting. ( H - J ) UMUC14, T24 and 5637 cells were treated with con siRNA, EMP1 siRNA, oxaliplatin (OXP, 50 µg/ml), or EMP1 siRNA + OXP. Cell viability was measured by CCK8 assay

Article Snippet: Primary antibodies against EMP1 (1:1000, Proteintech), SLC26A8 (1:1000, ABclonal) and β-actin (1:5000, Proteintech) were used.

Techniques: Comparison, Expressing, Western Blot, CCK-8 Assay

Fig. 1 The TME infiltration landscape, expression signature, and prognosis of EMP1 in breast cancer. A Schematic diagram of the correlation analysis between EMP1 expression and different tumor microenvironments (TMEs) with regard to cell infiltration. B Correlation between EMP1 expression and the infiltration of different TME-related cell types. C The TME cell-infiltrating landscape in BC patients with high or low EMP1 expression. D Gene expression correlation analysis between EMP1 and the classic CAF biomarkers in the TCGA_BRCA cohort. E Expression analysis of EMP1 in different PAM50 subtypes of BC. F, G BC patients with relatively high EMP1 expression possessed shorter overall survival and disease-free survival times. H, I Overall survival and disease-free survival of patients with BC. Higher EMP1 expression in patients with BC did not correlate with overall or disease-free survival. J Survival analysis of EMP1 for each PAM50 subtype in patients with BC.

Journal: Cell death & disease

Article Title: Tumor cell-derived EMP1 is essential for cancer-associated fibroblast infiltration in tumor microenvironment of triple-negative breast cancer.

doi: 10.1038/s41419-025-07464-9

Figure Lengend Snippet: Fig. 1 The TME infiltration landscape, expression signature, and prognosis of EMP1 in breast cancer. A Schematic diagram of the correlation analysis between EMP1 expression and different tumor microenvironments (TMEs) with regard to cell infiltration. B Correlation between EMP1 expression and the infiltration of different TME-related cell types. C The TME cell-infiltrating landscape in BC patients with high or low EMP1 expression. D Gene expression correlation analysis between EMP1 and the classic CAF biomarkers in the TCGA_BRCA cohort. E Expression analysis of EMP1 in different PAM50 subtypes of BC. F, G BC patients with relatively high EMP1 expression possessed shorter overall survival and disease-free survival times. H, I Overall survival and disease-free survival of patients with BC. Higher EMP1 expression in patients with BC did not correlate with overall or disease-free survival. J Survival analysis of EMP1 for each PAM50 subtype in patients with BC.

Article Snippet: The additional antibodies used in this study included EMP1 (Cat# sc-13133, Santa Cruz, Dallas, TX, USA), NFκB (P65) (Cat# sc-7304, Santa Cruz, Dallas, TX, USA), p-IκBα and total IκBα (Cat# sc-8007, Santa Cruz, Dallas, TX, USA), IL6 (Cat# sc- 56196, Santa Cruz, Dallas, TX, USA), FSP-1 (Cat# T40044, Abmart, Shanghai, China), monoclonal mouse anti-β-actin (1:5000 dilution, Cat# AF7018, Affinity, Liyang, China), and secondary antibody-goat antiRabbit & Mouse (Cat# M21003, Abmart, Shanghai, China).

Techniques: Expressing, Gene Expression

Fig. 2 EMP1 was highly expressed and correlated with CAF infiltration in TNBC. A Identification and classification of different subtypes of BC (N = 74) based on the immunohistochemical results using PR, ER, HER2, Ki-67, and CK5/6 antibodies. A total of 14 patients with lumina A type, 16 with of lumina B type, 15 with HER2+ type, and 24 with TNBC type were identified in our BC cohort. B EMP1 and αSMA protein levels were evaluated in the BC cohort using IHC staining. Expression analysis of EMP1 and αSMA in each subtype of BC was conducted. C The protein levels of EMP1 were significantly positively correlated with the protein levels of αSMA in BC (N = 74). D EMP1 mRNA expression was highly co-expressed with ACTA2 mRNA expression in the TCGA_BRCA cohort. E Observation of the expression patterns of EMP1 and αSMA in different subtypes of BC using serial pathological sections. ****P < 0.0001; ***P < 0.001; **P < 0.01; *P < 0.05.

Journal: Cell death & disease

Article Title: Tumor cell-derived EMP1 is essential for cancer-associated fibroblast infiltration in tumor microenvironment of triple-negative breast cancer.

doi: 10.1038/s41419-025-07464-9

Figure Lengend Snippet: Fig. 2 EMP1 was highly expressed and correlated with CAF infiltration in TNBC. A Identification and classification of different subtypes of BC (N = 74) based on the immunohistochemical results using PR, ER, HER2, Ki-67, and CK5/6 antibodies. A total of 14 patients with lumina A type, 16 with of lumina B type, 15 with HER2+ type, and 24 with TNBC type were identified in our BC cohort. B EMP1 and αSMA protein levels were evaluated in the BC cohort using IHC staining. Expression analysis of EMP1 and αSMA in each subtype of BC was conducted. C The protein levels of EMP1 were significantly positively correlated with the protein levels of αSMA in BC (N = 74). D EMP1 mRNA expression was highly co-expressed with ACTA2 mRNA expression in the TCGA_BRCA cohort. E Observation of the expression patterns of EMP1 and αSMA in different subtypes of BC using serial pathological sections. ****P < 0.0001; ***P < 0.001; **P < 0.01; *P < 0.05.

Article Snippet: The additional antibodies used in this study included EMP1 (Cat# sc-13133, Santa Cruz, Dallas, TX, USA), NFκB (P65) (Cat# sc-7304, Santa Cruz, Dallas, TX, USA), p-IκBα and total IκBα (Cat# sc-8007, Santa Cruz, Dallas, TX, USA), IL6 (Cat# sc- 56196, Santa Cruz, Dallas, TX, USA), FSP-1 (Cat# T40044, Abmart, Shanghai, China), monoclonal mouse anti-β-actin (1:5000 dilution, Cat# AF7018, Affinity, Liyang, China), and secondary antibody-goat antiRabbit & Mouse (Cat# M21003, Abmart, Shanghai, China).

Techniques: Immunohistochemical staining, Immunohistochemistry, Expressing

Fig. 3 EMP1 exerts oncogenic properties in TNBC cell lines. A The HE staining and IHC assay (EMP1) from the same donor were verified in TNBC patients. The paracancerous tissue in the left panel (normal duct tissue) and in the right panel (normal lobules of breast tissue). IHC staining results showed that EMP1 expression was upregulated in TNBC tissues. B The expression pattern of EMP1 in different BC cell lines was determined using quantitative RT-PCR assay. C, D Multiple monoclonal cell lines with EMP1 knockdown were screened using quantitative RT- PCR and western blotting assays. E, F The CCK-8 and colony formation assays verified that EMP1 knockdown suppressed the proliferation of the TNBC cell lines. G, H The transwell migration and invasion assays showed that EMP1 knockdown significantly inhibited the migration and invasion of the TNBC cell lines. I EMP1 was overexpressed in TNBC cell line MDA-MB-453. J, K The CCK-8 and colony formation assays verified that EMP1 overexpression promoted the proliferation of the TNBC cells. L The transwell migration and invasion assays showed that EMP1 overexpression significantly facilitated the migration and invasion of the TNBC cells. **P < 0.01.

Journal: Cell death & disease

Article Title: Tumor cell-derived EMP1 is essential for cancer-associated fibroblast infiltration in tumor microenvironment of triple-negative breast cancer.

doi: 10.1038/s41419-025-07464-9

Figure Lengend Snippet: Fig. 3 EMP1 exerts oncogenic properties in TNBC cell lines. A The HE staining and IHC assay (EMP1) from the same donor were verified in TNBC patients. The paracancerous tissue in the left panel (normal duct tissue) and in the right panel (normal lobules of breast tissue). IHC staining results showed that EMP1 expression was upregulated in TNBC tissues. B The expression pattern of EMP1 in different BC cell lines was determined using quantitative RT-PCR assay. C, D Multiple monoclonal cell lines with EMP1 knockdown were screened using quantitative RT- PCR and western blotting assays. E, F The CCK-8 and colony formation assays verified that EMP1 knockdown suppressed the proliferation of the TNBC cell lines. G, H The transwell migration and invasion assays showed that EMP1 knockdown significantly inhibited the migration and invasion of the TNBC cell lines. I EMP1 was overexpressed in TNBC cell line MDA-MB-453. J, K The CCK-8 and colony formation assays verified that EMP1 overexpression promoted the proliferation of the TNBC cells. L The transwell migration and invasion assays showed that EMP1 overexpression significantly facilitated the migration and invasion of the TNBC cells. **P < 0.01.

Article Snippet: The additional antibodies used in this study included EMP1 (Cat# sc-13133, Santa Cruz, Dallas, TX, USA), NFκB (P65) (Cat# sc-7304, Santa Cruz, Dallas, TX, USA), p-IκBα and total IκBα (Cat# sc-8007, Santa Cruz, Dallas, TX, USA), IL6 (Cat# sc- 56196, Santa Cruz, Dallas, TX, USA), FSP-1 (Cat# T40044, Abmart, Shanghai, China), monoclonal mouse anti-β-actin (1:5000 dilution, Cat# AF7018, Affinity, Liyang, China), and secondary antibody-goat antiRabbit & Mouse (Cat# M21003, Abmart, Shanghai, China).

Techniques: Staining, Immunohistochemistry, Expressing, Quantitative RT-PCR, Knockdown, Western Blot, CCK-8 Assay, Migration, Over Expression

Fig. 4 EMP1 depletion inhibited the proliferation and metastasis of xenograft tumors. A Morphology of tumor-bearing nude mice in the EMP1 knockdown and control groups. B Morphological differences in subcutaneous breast transplant tumors between the EMP1 knockdown and the control groups in nude mice. C The weight of transplanted tumors formed by TNBC cells in the EMP1 knockdown and control groups. D Volume growth curves of transplanted tumors between the EMP1 knockdown and the control groups. E Differences in body weight between the EMP1 knockdown group and the control group in nude mice. F Immunohistochemical staining results of EMP1 and αSMA in xenograft tumors in the EMP1 knockdown and control groups. G Observation of the number of metastatic foci formed by TNBC cells in the EMP1 knockdown and control groups in nude mice using a tail vein metastasis model. H Knockdown of EMP1 significantly inhibits the metastasis of TNBC cells in the liver, lung, and kidney organs of nude mice. **P < 0.01.

Journal: Cell death & disease

Article Title: Tumor cell-derived EMP1 is essential for cancer-associated fibroblast infiltration in tumor microenvironment of triple-negative breast cancer.

doi: 10.1038/s41419-025-07464-9

Figure Lengend Snippet: Fig. 4 EMP1 depletion inhibited the proliferation and metastasis of xenograft tumors. A Morphology of tumor-bearing nude mice in the EMP1 knockdown and control groups. B Morphological differences in subcutaneous breast transplant tumors between the EMP1 knockdown and the control groups in nude mice. C The weight of transplanted tumors formed by TNBC cells in the EMP1 knockdown and control groups. D Volume growth curves of transplanted tumors between the EMP1 knockdown and the control groups. E Differences in body weight between the EMP1 knockdown group and the control group in nude mice. F Immunohistochemical staining results of EMP1 and αSMA in xenograft tumors in the EMP1 knockdown and control groups. G Observation of the number of metastatic foci formed by TNBC cells in the EMP1 knockdown and control groups in nude mice using a tail vein metastasis model. H Knockdown of EMP1 significantly inhibits the metastasis of TNBC cells in the liver, lung, and kidney organs of nude mice. **P < 0.01.

Article Snippet: The additional antibodies used in this study included EMP1 (Cat# sc-13133, Santa Cruz, Dallas, TX, USA), NFκB (P65) (Cat# sc-7304, Santa Cruz, Dallas, TX, USA), p-IκBα and total IκBα (Cat# sc-8007, Santa Cruz, Dallas, TX, USA), IL6 (Cat# sc- 56196, Santa Cruz, Dallas, TX, USA), FSP-1 (Cat# T40044, Abmart, Shanghai, China), monoclonal mouse anti-β-actin (1:5000 dilution, Cat# AF7018, Affinity, Liyang, China), and secondary antibody-goat antiRabbit & Mouse (Cat# M21003, Abmart, Shanghai, China).

Techniques: Knockdown, Control, Immunohistochemical staining, Staining

Fig. 5 EMP1 knockdown in TNBC cells impaired the proliferation of CAFs. A Morphology of CAF cells isolated from the surgical resection tissue of a TNBC patient. B Schematic diagram of the cell co-cultivation system for different experimental groups, including CAF (empty), CAF + sh-NC_TNBC cell line (sh-NC), and CAF+sh-EMP1_TNBC cell line (sh-EMP1). C, D The growth rate of CAFs in the cell co-cultivation system of different experimental groups was determined using the CCK-8 assay. E, F The cell cycle distribution of CAFs in the cell co-cultivation system of different experimental groups was determined by flow cytometry. G, H The cell proliferation rate of CAFs in the cell co-cultivation system of different experimental groups was determined using the EdU assay. *P < 0.05; **P < 0.01.

Journal: Cell death & disease

Article Title: Tumor cell-derived EMP1 is essential for cancer-associated fibroblast infiltration in tumor microenvironment of triple-negative breast cancer.

doi: 10.1038/s41419-025-07464-9

Figure Lengend Snippet: Fig. 5 EMP1 knockdown in TNBC cells impaired the proliferation of CAFs. A Morphology of CAF cells isolated from the surgical resection tissue of a TNBC patient. B Schematic diagram of the cell co-cultivation system for different experimental groups, including CAF (empty), CAF + sh-NC_TNBC cell line (sh-NC), and CAF+sh-EMP1_TNBC cell line (sh-EMP1). C, D The growth rate of CAFs in the cell co-cultivation system of different experimental groups was determined using the CCK-8 assay. E, F The cell cycle distribution of CAFs in the cell co-cultivation system of different experimental groups was determined by flow cytometry. G, H The cell proliferation rate of CAFs in the cell co-cultivation system of different experimental groups was determined using the EdU assay. *P < 0.05; **P < 0.01.

Article Snippet: The additional antibodies used in this study included EMP1 (Cat# sc-13133, Santa Cruz, Dallas, TX, USA), NFκB (P65) (Cat# sc-7304, Santa Cruz, Dallas, TX, USA), p-IκBα and total IκBα (Cat# sc-8007, Santa Cruz, Dallas, TX, USA), IL6 (Cat# sc- 56196, Santa Cruz, Dallas, TX, USA), FSP-1 (Cat# T40044, Abmart, Shanghai, China), monoclonal mouse anti-β-actin (1:5000 dilution, Cat# AF7018, Affinity, Liyang, China), and secondary antibody-goat antiRabbit & Mouse (Cat# M21003, Abmart, Shanghai, China).

Techniques: Knockdown, Isolation, CCK-8 Assay, Cytometry, EdU Assay

Fig. 6 EMP1 was required for CAF infiltration in xenografts. A, B A mixture of TNBC cells and CAFs was injected subcutaneously into the mammary gland of nude mice, and the morphology and weight of the xenograft tumors formed by TNBC cells are shown in the plots. C Tumor volume growth curve of xenograft tumors in the CAF+ sh-NC_TNBC cell line (sh-NC) and the CAF+ sh-EMP1_TNBC cell line (sh-EMP1) groups. D The body weight of mice in the CAF+ sh-NC_TNBC cell line (sh-NC) group and the CAF+ sh-EMP1_TNBC cell line (sh-EMP1) group. E The expression of CAF biomarkers in xenograft tumors was determined by western blotting assay. F The CAF infiltration level in xenograft tumors is examined by IHC, Masson, and Sirius Red staining assays. G Knockdown of EMP1 in TNBC cells significantly inhibited CAF infiltration in xenograft tumors. Multicolor immunofluorescence experiments were performed in the xenograft tumors between sh-NC + CAF group and sh-EMP1 + CAF group. The CAFs are labeled by fibroblast biomarker anti-α-SMA with green fluorescence. The EMP1 expression in xenograft tumors was evaluated using anti-EMP1 bodies with red fluorescence. **P < 0.01.

Journal: Cell death & disease

Article Title: Tumor cell-derived EMP1 is essential for cancer-associated fibroblast infiltration in tumor microenvironment of triple-negative breast cancer.

doi: 10.1038/s41419-025-07464-9

Figure Lengend Snippet: Fig. 6 EMP1 was required for CAF infiltration in xenografts. A, B A mixture of TNBC cells and CAFs was injected subcutaneously into the mammary gland of nude mice, and the morphology and weight of the xenograft tumors formed by TNBC cells are shown in the plots. C Tumor volume growth curve of xenograft tumors in the CAF+ sh-NC_TNBC cell line (sh-NC) and the CAF+ sh-EMP1_TNBC cell line (sh-EMP1) groups. D The body weight of mice in the CAF+ sh-NC_TNBC cell line (sh-NC) group and the CAF+ sh-EMP1_TNBC cell line (sh-EMP1) group. E The expression of CAF biomarkers in xenograft tumors was determined by western blotting assay. F The CAF infiltration level in xenograft tumors is examined by IHC, Masson, and Sirius Red staining assays. G Knockdown of EMP1 in TNBC cells significantly inhibited CAF infiltration in xenograft tumors. Multicolor immunofluorescence experiments were performed in the xenograft tumors between sh-NC + CAF group and sh-EMP1 + CAF group. The CAFs are labeled by fibroblast biomarker anti-α-SMA with green fluorescence. The EMP1 expression in xenograft tumors was evaluated using anti-EMP1 bodies with red fluorescence. **P < 0.01.

Article Snippet: The additional antibodies used in this study included EMP1 (Cat# sc-13133, Santa Cruz, Dallas, TX, USA), NFκB (P65) (Cat# sc-7304, Santa Cruz, Dallas, TX, USA), p-IκBα and total IκBα (Cat# sc-8007, Santa Cruz, Dallas, TX, USA), IL6 (Cat# sc- 56196, Santa Cruz, Dallas, TX, USA), FSP-1 (Cat# T40044, Abmart, Shanghai, China), monoclonal mouse anti-β-actin (1:5000 dilution, Cat# AF7018, Affinity, Liyang, China), and secondary antibody-goat antiRabbit & Mouse (Cat# M21003, Abmart, Shanghai, China).

Techniques: Injection, Expressing, Western Blot, Staining, Knockdown, Labeling, Biomarker Discovery

Fig. 7 EMP1 knockdown inhibited TNBC progression through the NF-κB signaling pathway. A, B The RNA-seq studies were conducted in the MDA-MB-231 cell lines with or without EMP1 knockdown. The DEGs after EMP1 depletion were shown in the volcano map and heat plot. C The GO/KEGG analysis was performed using the DEGs from the EMP1 knockdown experiment. D Western blotting assay confirmed that EMP1 knockdown activates the NF-κB/IL6 axis in TNBC cell lines. E The IHC assay of RelA/p65 and IκBα was conducted in xenograft tumors formed by TNBC cell lines with or without EMP1 knockdown. F The expression level of IκBα can be restored by recombinant active TNFα protein (10 ng/ mL). G The rescue western blotting assay confirmed that EMP1 knockdown inhibited NF-κB signaling through upregulating expression of IκBα. H, I The rescue colony formation assay verified that EMP1 knockdown inhibited TNBC cell proliferation through IκBα/NF-κB signaling.

Journal: Cell death & disease

Article Title: Tumor cell-derived EMP1 is essential for cancer-associated fibroblast infiltration in tumor microenvironment of triple-negative breast cancer.

doi: 10.1038/s41419-025-07464-9

Figure Lengend Snippet: Fig. 7 EMP1 knockdown inhibited TNBC progression through the NF-κB signaling pathway. A, B The RNA-seq studies were conducted in the MDA-MB-231 cell lines with or without EMP1 knockdown. The DEGs after EMP1 depletion were shown in the volcano map and heat plot. C The GO/KEGG analysis was performed using the DEGs from the EMP1 knockdown experiment. D Western blotting assay confirmed that EMP1 knockdown activates the NF-κB/IL6 axis in TNBC cell lines. E The IHC assay of RelA/p65 and IκBα was conducted in xenograft tumors formed by TNBC cell lines with or without EMP1 knockdown. F The expression level of IκBα can be restored by recombinant active TNFα protein (10 ng/ mL). G The rescue western blotting assay confirmed that EMP1 knockdown inhibited NF-κB signaling through upregulating expression of IκBα. H, I The rescue colony formation assay verified that EMP1 knockdown inhibited TNBC cell proliferation through IκBα/NF-κB signaling.

Article Snippet: The additional antibodies used in this study included EMP1 (Cat# sc-13133, Santa Cruz, Dallas, TX, USA), NFκB (P65) (Cat# sc-7304, Santa Cruz, Dallas, TX, USA), p-IκBα and total IκBα (Cat# sc-8007, Santa Cruz, Dallas, TX, USA), IL6 (Cat# sc- 56196, Santa Cruz, Dallas, TX, USA), FSP-1 (Cat# T40044, Abmart, Shanghai, China), monoclonal mouse anti-β-actin (1:5000 dilution, Cat# AF7018, Affinity, Liyang, China), and secondary antibody-goat antiRabbit & Mouse (Cat# M21003, Abmart, Shanghai, China).

Techniques: Knockdown, RNA Sequencing, Western Blot, Expressing, Recombinant, Colony Assay

Fig. 8 EMP1 promoted CAF infiltration by enhancing IL6 secretion in TNBC cells. A The microporous membrane of the cell co-culture system only allows small molecules, such as secreted proteins, to pass through, and cells are too large to pass through the membrane. B EMP1 knockdown in TNBC cells suppressed the expression of αSMA in CAFs co-cultured with the corresponding TNBC cell lines. C EMP1 knockdown in TNBC cells suppressed the expression of αSMA and FSP-1 in CAFs co-cultured with corresponding TNBC cell lines. D ELISA assay confirmed that EMP1 knockdown decreased IL6 secretion in TNBC cell lines. E ELISA assay confirmed that EMP1 knockdown had no obvious effect on TNFα secretion in TNBC cell lines. F, G Recombinant active IL6 protein (10 ng/mL) rescued αSMA expression and increased active Akt expression in CAFs. H The IL6 protein level in xenograft tumors formed by TNBC cell lines with or without EMP1 knockdown was determined using an IHC assay. I The IL6 level in xenograft blood between mice in the EMP1 knockdown and the control groups were determined using ELISA. J The IL6 level in the blood of healthy volunteers (N = 10), non-TNBC breast cancer patients (N = 10), and TNBC patients (N = 6).

Journal: Cell death & disease

Article Title: Tumor cell-derived EMP1 is essential for cancer-associated fibroblast infiltration in tumor microenvironment of triple-negative breast cancer.

doi: 10.1038/s41419-025-07464-9

Figure Lengend Snippet: Fig. 8 EMP1 promoted CAF infiltration by enhancing IL6 secretion in TNBC cells. A The microporous membrane of the cell co-culture system only allows small molecules, such as secreted proteins, to pass through, and cells are too large to pass through the membrane. B EMP1 knockdown in TNBC cells suppressed the expression of αSMA in CAFs co-cultured with the corresponding TNBC cell lines. C EMP1 knockdown in TNBC cells suppressed the expression of αSMA and FSP-1 in CAFs co-cultured with corresponding TNBC cell lines. D ELISA assay confirmed that EMP1 knockdown decreased IL6 secretion in TNBC cell lines. E ELISA assay confirmed that EMP1 knockdown had no obvious effect on TNFα secretion in TNBC cell lines. F, G Recombinant active IL6 protein (10 ng/mL) rescued αSMA expression and increased active Akt expression in CAFs. H The IL6 protein level in xenograft tumors formed by TNBC cell lines with or without EMP1 knockdown was determined using an IHC assay. I The IL6 level in xenograft blood between mice in the EMP1 knockdown and the control groups were determined using ELISA. J The IL6 level in the blood of healthy volunteers (N = 10), non-TNBC breast cancer patients (N = 10), and TNBC patients (N = 6).

Article Snippet: The additional antibodies used in this study included EMP1 (Cat# sc-13133, Santa Cruz, Dallas, TX, USA), NFκB (P65) (Cat# sc-7304, Santa Cruz, Dallas, TX, USA), p-IκBα and total IκBα (Cat# sc-8007, Santa Cruz, Dallas, TX, USA), IL6 (Cat# sc- 56196, Santa Cruz, Dallas, TX, USA), FSP-1 (Cat# T40044, Abmart, Shanghai, China), monoclonal mouse anti-β-actin (1:5000 dilution, Cat# AF7018, Affinity, Liyang, China), and secondary antibody-goat antiRabbit & Mouse (Cat# M21003, Abmart, Shanghai, China).

Techniques: Membrane, Co-Culture Assay, Knockdown, Expressing, Cell Culture, Enzyme-linked Immunosorbent Assay, Recombinant, Control

Fig. 9 EMP1 promotes TNBC progression and metastasis by mediating cell-cell communication between cancer cells and CAFs and enhancing CAF infiltration.

Journal: Cell death & disease

Article Title: Tumor cell-derived EMP1 is essential for cancer-associated fibroblast infiltration in tumor microenvironment of triple-negative breast cancer.

doi: 10.1038/s41419-025-07464-9

Figure Lengend Snippet: Fig. 9 EMP1 promotes TNBC progression and metastasis by mediating cell-cell communication between cancer cells and CAFs and enhancing CAF infiltration.

Article Snippet: The additional antibodies used in this study included EMP1 (Cat# sc-13133, Santa Cruz, Dallas, TX, USA), NFκB (P65) (Cat# sc-7304, Santa Cruz, Dallas, TX, USA), p-IκBα and total IκBα (Cat# sc-8007, Santa Cruz, Dallas, TX, USA), IL6 (Cat# sc- 56196, Santa Cruz, Dallas, TX, USA), FSP-1 (Cat# T40044, Abmart, Shanghai, China), monoclonal mouse anti-β-actin (1:5000 dilution, Cat# AF7018, Affinity, Liyang, China), and secondary antibody-goat antiRabbit & Mouse (Cat# M21003, Abmart, Shanghai, China).

Techniques: