antibodies gpx2 antibody  (Bioss)

Journal: Frontiers in Immunology

Article Title: GPX2+ tumor cells recruit LGALS1+ B cells via CCL26-CCR3 axis to promote immunosuppression and tumor progression in hepatocellular carcinoma

doi: 10.3389/fimmu.2026.1709855

Figure Lengend Snippet: Characterization and functional profiling of distinct tumor cell populations in HBV-negative and HBV-positive hepatocellular carcinoma. (A) UMAP visualization of scRNA-seq data from tumor cells across all HCC samples, color-coded by clusters. Clusters were annotated according to cluster-specific marker genes shown in (B) . (B) Heatmap of representative marker genes for each major cluster. (C) UMAP visualization of tumor cells from all HCC samples, color-coded by subpopulation identity. (D) Distribution of distinct tumor cell subpopulations in HBV-negative and HBV-positive HCC. (E) Bar plot showing the relative abundance of tumor cell subpopulations in HBV-negative versus HBV-positive HCC. (F) GO enrichment analysis of characteristic genes from GPX2 + tumor cell subpopulations. (G) KEGG enrichment analysis of characteristic genes from GPX2 + tumor cell subpopulations.

Article Snippet: Immunohistochemistry (IHC) images of GPX2 in HCC tissues were retrieved from the Human Protein Atlas (HPA; http://www.proteinatlas.org/ ).

Techniques: Functional Assay, Marker

Journal: Frontiers in Immunology

Article Title: GPX2+ tumor cells recruit LGALS1+ B cells via CCL26-CCR3 axis to promote immunosuppression and tumor progression in hepatocellular carcinoma

doi: 10.3389/fimmu.2026.1709855

Figure Lengend Snippet: GPX2 drives the expression of stemness-associated features in hepatocellular carcinoma cells. (A) mRNA and protein expression of GPX2 in tumor and normal tissues from the TCGA and GTEx datasets. (B) Representative IHC images showing differential GPX2 expression from the Human Protein Atlas (HPA). (C) Quantification of GPX2 protein expression by IHC in cour cohort. (D) GPX2 protein levels in surgically resected clinical samples, with Tubulin as the loading control. (E) Quantification of GPX2 protein expression. (F) GPX2 mRNA levels in clinical HCC samples. (G) GPX2 protein expression in HBV-negative versus HBV-positive HCC tissues. (H) GPX2 mRNA expression in HBV-negative versus HBV-positive HCC tissues. (I) Expression of stemness-associated markers (MYC, ALDH1A1, CXCR4, CD44) across tumor cell subtypes at the single-cell level. (J) Correlation analysis between GPX2 and stemness-related markers (MYC, CD44, CXCR4, ALDH1A1) in the TCGA-LIHC cohort. (K) GPX2 expression across multiple tumor types in the TCGA dataset. (L) Representative H&E and IHC staining of GPX2, c-MYC, CD44, and ALDH1A1 in clinical samples. (M) Correlation analysis of GPX2 with MYC, ALDH1A1, and CD44 expression in clinical HCC tissues. *** P<0.001.

Article Snippet: Immunohistochemistry (IHC) images of GPX2 in HCC tissues were retrieved from the Human Protein Atlas (HPA; http://www.proteinatlas.org/ ).

Techniques: Expressing, Control, Single Cell, Immunohistochemistry

Journal: Frontiers in Immunology

Article Title: GPX2+ tumor cells recruit LGALS1+ B cells via CCL26-CCR3 axis to promote immunosuppression and tumor progression in hepatocellular carcinoma

doi: 10.3389/fimmu.2026.1709855

Figure Lengend Snippet: GPX2 promotes malignant phenotypes and cancer stem cell properties in HBV-positive hepatocellular carcinoma. (A, B) Western blot analysis confirming GPX2 overexpression and knockdown efficiency in MHCC97H (A) and Hep3B (B) cells. (C) qPCR validation of GPX2 overexpression efficiency at the mRNA level in MHCC97H and Hep3B cells. (D) qPCR validation of GPX2 knockdown efficiency at the mRNA level in MHCC97H and Hep3B cells. (E) Alterations in stemness-related gene expression following GPX2 overexpression in MHCC97H and Hep3B cells. (F) Alterations in stemness-related gene expression following GPX2 knockdown in MHCC97H and Hep3B cells. (G) Cell proliferation rates in MHCC97H and Hep3B cells after GPX2 overexpression. (H) Cell proliferation rates in MHCC97H and Hep3B cells after GPX2 knockdown. (I, J) Sphere formation capacity and quantification in MHCC97H and Hep3B cells upon GPX2 overexpression (I) or knockdown (J) . (K) PI staining assay assessing cisplatin sensitivity in GPX2-overexpressing or knockdown cells. (L, M) Migration capacity and quantification in MHCC97H and Hep3B cells following GPX2 overexpression (L) or knockdown (M) . *** P<0.001.

Article Snippet: Immunohistochemistry (IHC) images of GPX2 in HCC tissues were retrieved from the Human Protein Atlas (HPA; http://www.proteinatlas.org/ ).

Techniques: Western Blot, Over Expression, Knockdown, Biomarker Discovery, Gene Expression, Staining, Migration

Journal: Frontiers in Immunology

Article Title: GPX2+ tumor cells recruit LGALS1+ B cells via CCL26-CCR3 axis to promote immunosuppression and tumor progression in hepatocellular carcinoma

doi: 10.3389/fimmu.2026.1709855

Figure Lengend Snippet: GPX2 promotes hepatocellular carcinoma stemness via the ROS–MYC signaling axis. (A) Volcano plot showing differentially expressed genes (DEGs) between GPX2-high and GPX2-low groups in the TCGA-LIHC dataset. (B, C) GO (B) and KEGG (C) enrichment analyses of upregulated DEGs in GPX2-high tumors. (D) Protein–protein interaction (PPI) network of GPX2 and related redox-associated proteins. (E) Intracellular ROS levels in MHCC97H and Hep3B cells. (F) Expression of stemness-associated markers in control (Vector), GPX2-overexpressing, and GPX2-overexpressing cells treated with the ROS agonist Vandetanib. (G) Expression of stemness-associated markers in control (shNC), GPX2-knockdown, and GPX2-knockdown cells treated with the ROS scavenger NAC. (H) Sphere-forming capacity of Vector, GPX2-overexpressing, and GPX2-overexpressing cells with Vandetanib treatment. (I) Sphere-forming capacity of shNC, GPX2-knockdown, and GPX2-knockdown cells with NAC treatment.

Article Snippet: Immunohistochemistry (IHC) images of GPX2 in HCC tissues were retrieved from the Human Protein Atlas (HPA; http://www.proteinatlas.org/ ).

Techniques: Expressing, Control, Plasmid Preparation, Knockdown

Journal: Frontiers in Immunology

Article Title: GPX2+ tumor cells recruit LGALS1+ B cells via CCL26-CCR3 axis to promote immunosuppression and tumor progression in hepatocellular carcinoma

doi: 10.3389/fimmu.2026.1709855

Figure Lengend Snippet: GPX2 promotes hepatocellular carcinoma stemness via the ROS–MYC signaling axis. (A) Immunofluorescence images showing intracellular localization of MYC in Vector, GPX2-overexpressing, and GPX2-overexpressing cells treated with the ROS agonist Vandetanib. (B–D) Correlation analysis between MYC and stemness-associated markers (CD90, CD44, ALDH1A1) in the TCGA-LIHC dataset. (E) Knockdown efficiency of MYC in MHCC97H and Hep3B cells. (F) Rescue experiments in Vector and GPX2-overexpressing cells transfected with siNC or siMYC, showing mRNA expression of stemness-associated markers. (G) Overexpression efficiency of MYC in MHCC97H and Hep3B cells. (H) Rescue experiments in Vector and GPX2-overexpressing cells transfected with MYC-Vector or MYC-overexpression plasmids, showing mRNA expression of stemness-associated markers. (I) Sphere formation assays comparing Vector, GPX2-overexpressing cells transfected with siNC or siMYC. (J) Sphere formation assays comparing Vector, GPX2-overexpressing cells transfected with MYC-Vector or MYC-overexpression plasmids. (K) ChIP-qPCR Results of MYC Binding to the Promoter Regions of CD44, CD90, and ALDH1A1 in Hep3B Cells. *** P<0.001.

Article Snippet: Immunohistochemistry (IHC) images of GPX2 in HCC tissues were retrieved from the Human Protein Atlas (HPA; http://www.proteinatlas.org/ ).

Techniques: Immunofluorescence, Plasmid Preparation, Knockdown, Transfection, Expressing, Over Expression, ChIP-qPCR, Binding Assay

Journal: Frontiers in Immunology

Article Title: GPX2+ tumor cells recruit LGALS1+ B cells via CCL26-CCR3 axis to promote immunosuppression and tumor progression in hepatocellular carcinoma

doi: 10.3389/fimmu.2026.1709855

Figure Lengend Snippet: GPX2 promotes immune modulation in hepatocellular carcinoma through MYC-dependent induction of LGALS1 in B cells. (A) GO enrichment analysis (Biological Process) of genes upregulated in GPX2-high patients from the TCGA-LIHC cohort. (B) Bar plot showing proportions of different immune cell types in HBV-negative and HBV-positive HCC. (C) UMAP visualization of scRNA-seq data from B cells across all HCC samples, color-coded by subpopulation identity. (D) Heatmap of representative marker genes for major B-cell clusters. (E, F) Kaplan–Meier curves comparing overall survival (E) and disease-specific survival (F) between LGALS1-high and LGALS1-low patients in the TCGA-LIHC cohort. (G) Multiplex immunohistochemistry (mIHC) of HBV-negative and HBV-positive HCC tissues (blue, DAPI; yellow, GPX2; green, LGALS1; purple, CD79B). (H) Quantification of CD79B + LGALS1 + B cells per microscopic field. (I) Schematic illustration of the co-culture system for JM1 B cells and tumor cells. (J) qPCR analysis of LGALS1 expression in JM1 cells co-cultured with MHCC97H Vector, GPX2-overexpressing, or MYC-silenced tumor cells. (K) qPCR analysis of LGALS1 expression in JM1 cells co-cultured with MHCC97H shNC, GPX2-knockdown, or MYC-overexpressing tumor cells. *** P<0.001.

Article Snippet: Immunohistochemistry (IHC) images of GPX2 in HCC tissues were retrieved from the Human Protein Atlas (HPA; http://www.proteinatlas.org/ ).

Techniques: Marker, Multiplex Assay, Immunohistochemistry, Co-Culture Assay, Expressing, Cell Culture, Plasmid Preparation, Knockdown

Journal: Frontiers in Immunology

Article Title: GPX2+ tumor cells recruit LGALS1+ B cells via CCL26-CCR3 axis to promote immunosuppression and tumor progression in hepatocellular carcinoma

doi: 10.3389/fimmu.2026.1709855

Figure Lengend Snippet: GPX2–CCL26 axis promotes LGALS1 + B-cell accumulation and immune evasion in HBV-positive HCC. (A) CCL26 expression in tumor versus normal liver tissues from the TCGA-LIHC dataset. (B) Correlation between CCL26 expression and immune cell infiltration estimated by ImmuCellAI, showing positive associations with B cells, CD4 + T cells, CD8 + T cells, dendritic cells (DCs), and natural killer (NK) cells, and negative correlations with monocytes, neutrophils, and Th17 cells. (C) Correlation analysis between GPX2 and CCL26 expression in the TCGA-LIHC dataset. (D) qPCR analysis of CCL26 mRNA expression in MHCC97H and Hep3B cells with GPX2 overexpression or knockdown, with or without Vandetanib (ROS agonist) or NAC (ROS scavenger). (E) CCL26 mRNA Stability Analysis in MHCC97H and Hep3B Cell Lines via Half-life Measurement Assay. (F) LISA quantification of secreted CCL26 levels in culture supernatants. (G) Co-culture assays of JM1 B cells with MHCC97H cells: LGALS1 expression changes upon GPX2 modulation with or without recombinant CCL26, CCL26 neutralization, or CCR3 inhibition. (H) Flow Cytometric Quantification and Statistical Representation of IFN-γ Expression in Hepatoma Cells Following Co-culture with Jurkat Cells in Clinical Specimens. (I) qPCR of IFN-γ Expression in MHCC97H and Hep3B Cells Following Co-culture with Jurkat Cells. *** P<0.001.

Article Snippet: Immunohistochemistry (IHC) images of GPX2 in HCC tissues were retrieved from the Human Protein Atlas (HPA; http://www.proteinatlas.org/ ).

Techniques: Expressing, Over Expression, Knockdown, Co-Culture Assay, Recombinant, Neutralization, Inhibition

Journal: Frontiers in Immunology

Article Title: GPX2+ tumor cells recruit LGALS1+ B cells via CCL26-CCR3 axis to promote immunosuppression and tumor progression in hepatocellular carcinoma

doi: 10.3389/fimmu.2026.1709855

Figure Lengend Snippet: GPX2 drives tumor progression in vivo and B-Cell targeting potentiates anti-PD1-mediated elimination of GPX2-High expressing cells. (A) qPCR Detection of GPX2 Knockdown Efficiency in Hepa1–6 Cells. (B) Colony Formation Assay (96h) of Hepa1–6 Cells with GPX2 Knockdown and Control Groups. (C) Subcutaneous Tumor Xenograft Experiment Results of Hepa1–6 Cells with GPX2 Knockdown and Control Groups. (D) Tumor Growth Curves from the Subcutaneous Xenograft Assay of Hepa1–6 Cells with GPX2 Knockdown versus Control Groups. (E) Tumor Weight in Subcutaneous Xenograft Assay of Hepa1–6 Cells with GPX2 Knockdown versus Control Groups. (F) qPCR Detection of GPX2 Overexpression Efficiency in Hepa1–6 Cells. (G) Colony Formation Assay (96h) of Hepa1–6 Cells with GPX2 Overexpression and Control Groups. (H) Subcutaneous Tumor Xenograft Experiment Results of Hepa1–6 Cells with GPX2 Overexpression and Control Groups. (I) Tumor Growth Curves from the Subcutaneous Xenograft Assay of Hepa1–6 Cells with GPX2 Overexpression versus Control Groups. (J) Tumor Weight in Subcutaneous Xenograft Assay of Hepa1–6 Cells with GPX2 Overexpression versus Control Groups. (K) H&E and IHC (GPX2 and CD79B) Staining Results with Statistical Analysis of Subcutaneous Tumors from Hepa1–6 Cells with GPX2 Knockdown versus Control Groups. (L) H&E and IHC (GPX2 and CD79B) Staining Results with Statistical Analysis of Subcutaneous Tumors from Hepa1–6 Cells with GPX2 Overexpression versus Control Groups. (M) Schematic Diagram of the Animal Experiment Strategy. (N) Experimental Results of Subcutaneous Tumor Xenograft Assay with GPX2 Overexpression, Anti-PD1 Therapy, and Combination Treatment. (O) Tumor Growth Curves from Subcutaneous Xenograft Assays of GPX2 Overexpression, Anti-PD1 Therapy, and Combination Treatment. (P) Tumor Weight in Subcutaneous Xenograft Assay of GPX2 Overexpression, Anti-PD1 Therapy, and Combination Treatment. (Q) Flow Cytometry Analysis of Different Cell Sorting Strategies. (R) Analysis and Statistics of Infiltrating B Cells in GPX2 Overexpression, Anti-PD1 Therapy, and Combination Treatment. (S) Analysis and Statistics of Infiltrating Tex Cells in GPX2 Overexpression, Anti-PD1 Therapy, and Combination Treatment. (T) Analysis and Statistics of Infiltrating Treg Cells in GPX2 Overexpression, Anti-PD1 Therapy, and Combination Treatment. * represents P<0.05, ** represents P<0.01, *** represents P<0.001.

Article Snippet: Immunohistochemistry (IHC) images of GPX2 in HCC tissues were retrieved from the Human Protein Atlas (HPA; http://www.proteinatlas.org/ ).

Techniques: In Vivo, Expressing, Knockdown, Colony Assay, Control, Xenograft Assay, Over Expression, Staining, Flow Cytometry, FACS

Journal: Frontiers in Immunology

Article Title: GPX2+ tumor cells recruit LGALS1+ B cells via CCL26-CCR3 axis to promote immunosuppression and tumor progression in hepatocellular carcinoma

doi: 10.3389/fimmu.2026.1709855

Figure Lengend Snippet: Mechanistic model of GPX2–ROS–MYC axis in HBV + HCC. GPX2 reduces ROS to sustain MYC activity and CCL26 secretion, which induces immunosuppressive LGALS1 + B-cell differentiation.

Article Snippet: Immunohistochemistry (IHC) images of GPX2 in HCC tissues were retrieved from the Human Protein Atlas (HPA; http://www.proteinatlas.org/ ).

Techniques: Activity Assay, Cell Differentiation