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95
MedChemExpress cxcr2 blockade
TRIDENT induces chemotactic and polarizing signals that recruit and program neutrophils toward an antitumor phenotype. a Schematic of the in vitro Transwell assay evaluating neutrophil migration toward tumor-conditioned medium derived from the indicated treatments. b Quantification of neutrophil migration across Transwell membranes ( n = 4 per group). c Experimental design of the in vivo neutrophil-trafficking assay in a dual-tumor model after indicated therapy. d Representative flow cytometry plots and quantification of transferred CD45.1⁺ neutrophils in tumors ( n = 7 per group). e Single-cell RNA-seq showing <t>Cxcr2</t> upregulation in neutrophils from TRIDENT-treated tumors. Genes were classified as upregulated if increased in both comparisons, downregulated if decreased in both, oppositely regulated if significant in both but with opposite direction, and unchanged if non-significant in ≥1 comparison or showed minimal change. f Flow cytometric quantification of CXCR2⁺ neutrophils in second tumors in the LLC model across treatment groups ( n = 7 per group). g Heatmap comparing relative mRNA expression of Cxcl1, Cxcl2, Cxcl3 , and Cxcl5 from averaged qPCR values in tumor tissues after the indicated treatment ( n = 4 per group). Tumor growth curves ( h , i ) and survival curve ( j ) of LLC-bearing mice treated with TRIDENT alone or with CXCR2 blockade ( n = 9 per group). k, l qPCR analysis showing increased expression of Csf2 and Ifng in tumor tissues after indicated treatment ( n = 4 per group). m – p Flow cytometric analysis of antigen presentation and co-stimulatory molecules (CD14, ICAM-1, MHC-I, and CD86) on neutrophils cultured with tumor-conditioned medium derived from control, LDRT-, or HDRT-treated tumors ( n = 10 per group). Tumor growth curves ( q , r ) and survival curve ( s ) of LLC-bearing mice treated with TRIDENT alone or with GM-CSF/IFN-γ blockade ( n = 6 per group). Data are mean ± SEM. Statistical significance was assessed by one-way ANOVA ( b, f, g, k – p ), Student’s t test ( d ), two-way ANOVA ( h , i, q , r ) or log-rank test for survival ( j , s ). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001
Cxcr2 Blockade, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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TRIDENT induces chemotactic and polarizing signals that recruit and program neutrophils toward an antitumor phenotype. a Schematic of the in vitro Transwell assay evaluating neutrophil migration toward tumor-conditioned medium derived from the indicated treatments. b Quantification of neutrophil migration across Transwell membranes ( n = 4 per group). c Experimental design of the in vivo neutrophil-trafficking assay in a dual-tumor model after indicated therapy. d Representative flow cytometry plots and quantification of transferred CD45.1⁺ neutrophils in tumors ( n = 7 per group). e Single-cell RNA-seq showing <t>Cxcr2</t> upregulation in neutrophils from TRIDENT-treated tumors. Genes were classified as upregulated if increased in both comparisons, downregulated if decreased in both, oppositely regulated if significant in both but with opposite direction, and unchanged if non-significant in ≥1 comparison or showed minimal change. f Flow cytometric quantification of CXCR2⁺ neutrophils in second tumors in the LLC model across treatment groups ( n = 7 per group). g Heatmap comparing relative mRNA expression of Cxcl1, Cxcl2, Cxcl3 , and Cxcl5 from averaged qPCR values in tumor tissues after the indicated treatment ( n = 4 per group). Tumor growth curves ( h , i ) and survival curve ( j ) of LLC-bearing mice treated with TRIDENT alone or with CXCR2 blockade ( n = 9 per group). k, l qPCR analysis showing increased expression of Csf2 and Ifng in tumor tissues after indicated treatment ( n = 4 per group). m – p Flow cytometric analysis of antigen presentation and co-stimulatory molecules (CD14, ICAM-1, MHC-I, and CD86) on neutrophils cultured with tumor-conditioned medium derived from control, LDRT-, or HDRT-treated tumors ( n = 10 per group). Tumor growth curves ( q , r ) and survival curve ( s ) of LLC-bearing mice treated with TRIDENT alone or with GM-CSF/IFN-γ blockade ( n = 6 per group). Data are mean ± SEM. Statistical significance was assessed by one-way ANOVA ( b, f, g, k – p ), Student’s t test ( d ), two-way ANOVA ( h , i, q , r ) or log-rank test for survival ( j , s ). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001
Cd182 Cxcr2 Apc, supplied by Miltenyi Biotec, 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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cxcr2  (Bioss)
94
Bioss cxcr2
TRIDENT induces chemotactic and polarizing signals that recruit and program neutrophils toward an antitumor phenotype. a Schematic of the in vitro Transwell assay evaluating neutrophil migration toward tumor-conditioned medium derived from the indicated treatments. b Quantification of neutrophil migration across Transwell membranes ( n = 4 per group). c Experimental design of the in vivo neutrophil-trafficking assay in a dual-tumor model after indicated therapy. d Representative flow cytometry plots and quantification of transferred CD45.1⁺ neutrophils in tumors ( n = 7 per group). e Single-cell RNA-seq showing <t>Cxcr2</t> upregulation in neutrophils from TRIDENT-treated tumors. Genes were classified as upregulated if increased in both comparisons, downregulated if decreased in both, oppositely regulated if significant in both but with opposite direction, and unchanged if non-significant in ≥1 comparison or showed minimal change. f Flow cytometric quantification of CXCR2⁺ neutrophils in second tumors in the LLC model across treatment groups ( n = 7 per group). g Heatmap comparing relative mRNA expression of Cxcl1, Cxcl2, Cxcl3 , and Cxcl5 from averaged qPCR values in tumor tissues after the indicated treatment ( n = 4 per group). Tumor growth curves ( h , i ) and survival curve ( j ) of LLC-bearing mice treated with TRIDENT alone or with CXCR2 blockade ( n = 9 per group). k, l qPCR analysis showing increased expression of Csf2 and Ifng in tumor tissues after indicated treatment ( n = 4 per group). m – p Flow cytometric analysis of antigen presentation and co-stimulatory molecules (CD14, ICAM-1, MHC-I, and CD86) on neutrophils cultured with tumor-conditioned medium derived from control, LDRT-, or HDRT-treated tumors ( n = 10 per group). Tumor growth curves ( q , r ) and survival curve ( s ) of LLC-bearing mice treated with TRIDENT alone or with GM-CSF/IFN-γ blockade ( n = 6 per group). Data are mean ± SEM. Statistical significance was assessed by one-way ANOVA ( b, f, g, k – p ), Student’s t test ( d ), two-way ANOVA ( h , i, q , r ) or log-rank test for survival ( j , s ). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001
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MedChemExpress cxcr2 antagonist
TRIDENT induces chemotactic and polarizing signals that recruit and program neutrophils toward an antitumor phenotype. a Schematic of the in vitro Transwell assay evaluating neutrophil migration toward tumor-conditioned medium derived from the indicated treatments. b Quantification of neutrophil migration across Transwell membranes ( n = 4 per group). c Experimental design of the in vivo neutrophil-trafficking assay in a dual-tumor model after indicated therapy. d Representative flow cytometry plots and quantification of transferred CD45.1⁺ neutrophils in tumors ( n = 7 per group). e Single-cell RNA-seq showing <t>Cxcr2</t> upregulation in neutrophils from TRIDENT-treated tumors. Genes were classified as upregulated if increased in both comparisons, downregulated if decreased in both, oppositely regulated if significant in both but with opposite direction, and unchanged if non-significant in ≥1 comparison or showed minimal change. f Flow cytometric quantification of CXCR2⁺ neutrophils in second tumors in the LLC model across treatment groups ( n = 7 per group). g Heatmap comparing relative mRNA expression of Cxcl1, Cxcl2, Cxcl3 , and Cxcl5 from averaged qPCR values in tumor tissues after the indicated treatment ( n = 4 per group). Tumor growth curves ( h , i ) and survival curve ( j ) of LLC-bearing mice treated with TRIDENT alone or with CXCR2 blockade ( n = 9 per group). k, l qPCR analysis showing increased expression of Csf2 and Ifng in tumor tissues after indicated treatment ( n = 4 per group). m – p Flow cytometric analysis of antigen presentation and co-stimulatory molecules (CD14, ICAM-1, MHC-I, and CD86) on neutrophils cultured with tumor-conditioned medium derived from control, LDRT-, or HDRT-treated tumors ( n = 10 per group). Tumor growth curves ( q , r ) and survival curve ( s ) of LLC-bearing mice treated with TRIDENT alone or with GM-CSF/IFN-γ blockade ( n = 6 per group). Data are mean ± SEM. Statistical significance was assessed by one-way ANOVA ( b, f, g, k – p ), Student’s t test ( d ), two-way ANOVA ( h , i, q , r ) or log-rank test for survival ( j , s ). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001
Cxcr2 Antagonist, supplied by MedChemExpress, 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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MedChemExpress cxcr2 inhibitor sb225002
TRIDENT induces chemotactic and polarizing signals that recruit and program neutrophils toward an antitumor phenotype. a Schematic of the in vitro Transwell assay evaluating neutrophil migration toward tumor-conditioned medium derived from the indicated treatments. b Quantification of neutrophil migration across Transwell membranes ( n = 4 per group). c Experimental design of the in vivo neutrophil-trafficking assay in a dual-tumor model after indicated therapy. d Representative flow cytometry plots and quantification of transferred CD45.1⁺ neutrophils in tumors ( n = 7 per group). e Single-cell RNA-seq showing <t>Cxcr2</t> upregulation in neutrophils from TRIDENT-treated tumors. Genes were classified as upregulated if increased in both comparisons, downregulated if decreased in both, oppositely regulated if significant in both but with opposite direction, and unchanged if non-significant in ≥1 comparison or showed minimal change. f Flow cytometric quantification of CXCR2⁺ neutrophils in second tumors in the LLC model across treatment groups ( n = 7 per group). g Heatmap comparing relative mRNA expression of Cxcl1, Cxcl2, Cxcl3 , and Cxcl5 from averaged qPCR values in tumor tissues after the indicated treatment ( n = 4 per group). Tumor growth curves ( h , i ) and survival curve ( j ) of LLC-bearing mice treated with TRIDENT alone or with CXCR2 blockade ( n = 9 per group). k, l qPCR analysis showing increased expression of Csf2 and Ifng in tumor tissues after indicated treatment ( n = 4 per group). m – p Flow cytometric analysis of antigen presentation and co-stimulatory molecules (CD14, ICAM-1, MHC-I, and CD86) on neutrophils cultured with tumor-conditioned medium derived from control, LDRT-, or HDRT-treated tumors ( n = 10 per group). Tumor growth curves ( q , r ) and survival curve ( s ) of LLC-bearing mice treated with TRIDENT alone or with GM-CSF/IFN-γ blockade ( n = 6 per group). Data are mean ± SEM. Statistical significance was assessed by one-way ANOVA ( b, f, g, k – p ), Student’s t test ( d ), two-way ANOVA ( h , i, q , r ) or log-rank test for survival ( j , s ). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001
Cxcr2 Inhibitor Sb225002, supplied by MedChemExpress, 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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Pierre Fabre Group anti cxcr2 monoclonal
TRIDENT induces chemotactic and polarizing signals that recruit and program neutrophils toward an antitumor phenotype. a Schematic of the in vitro Transwell assay evaluating neutrophil migration toward tumor-conditioned medium derived from the indicated treatments. b Quantification of neutrophil migration across Transwell membranes ( n = 4 per group). c Experimental design of the in vivo neutrophil-trafficking assay in a dual-tumor model after indicated therapy. d Representative flow cytometry plots and quantification of transferred CD45.1⁺ neutrophils in tumors ( n = 7 per group). e Single-cell RNA-seq showing <t>Cxcr2</t> upregulation in neutrophils from TRIDENT-treated tumors. Genes were classified as upregulated if increased in both comparisons, downregulated if decreased in both, oppositely regulated if significant in both but with opposite direction, and unchanged if non-significant in ≥1 comparison or showed minimal change. f Flow cytometric quantification of CXCR2⁺ neutrophils in second tumors in the LLC model across treatment groups ( n = 7 per group). g Heatmap comparing relative mRNA expression of Cxcl1, Cxcl2, Cxcl3 , and Cxcl5 from averaged qPCR values in tumor tissues after the indicated treatment ( n = 4 per group). Tumor growth curves ( h , i ) and survival curve ( j ) of LLC-bearing mice treated with TRIDENT alone or with CXCR2 blockade ( n = 9 per group). k, l qPCR analysis showing increased expression of Csf2 and Ifng in tumor tissues after indicated treatment ( n = 4 per group). m – p Flow cytometric analysis of antigen presentation and co-stimulatory molecules (CD14, ICAM-1, MHC-I, and CD86) on neutrophils cultured with tumor-conditioned medium derived from control, LDRT-, or HDRT-treated tumors ( n = 10 per group). Tumor growth curves ( q , r ) and survival curve ( s ) of LLC-bearing mice treated with TRIDENT alone or with GM-CSF/IFN-γ blockade ( n = 6 per group). Data are mean ± SEM. Statistical significance was assessed by one-way ANOVA ( b, f, g, k – p ), Student’s t test ( d ), two-way ANOVA ( h , i, q , r ) or log-rank test for survival ( j , s ). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001
Anti Cxcr2 Monoclonal, supplied by Pierre Fabre Group, 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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MedChemExpress 2 1 2 cxcr2 pharmacological inhibition mice
TRIDENT induces chemotactic and polarizing signals that recruit and program neutrophils toward an antitumor phenotype. a Schematic of the in vitro Transwell assay evaluating neutrophil migration toward tumor-conditioned medium derived from the indicated treatments. b Quantification of neutrophil migration across Transwell membranes ( n = 4 per group). c Experimental design of the in vivo neutrophil-trafficking assay in a dual-tumor model after indicated therapy. d Representative flow cytometry plots and quantification of transferred CD45.1⁺ neutrophils in tumors ( n = 7 per group). e Single-cell RNA-seq showing <t>Cxcr2</t> upregulation in neutrophils from TRIDENT-treated tumors. Genes were classified as upregulated if increased in both comparisons, downregulated if decreased in both, oppositely regulated if significant in both but with opposite direction, and unchanged if non-significant in ≥1 comparison or showed minimal change. f Flow cytometric quantification of CXCR2⁺ neutrophils in second tumors in the LLC model across treatment groups ( n = 7 per group). g Heatmap comparing relative mRNA expression of Cxcl1, Cxcl2, Cxcl3 , and Cxcl5 from averaged qPCR values in tumor tissues after the indicated treatment ( n = 4 per group). Tumor growth curves ( h , i ) and survival curve ( j ) of LLC-bearing mice treated with TRIDENT alone or with CXCR2 blockade ( n = 9 per group). k, l qPCR analysis showing increased expression of Csf2 and Ifng in tumor tissues after indicated treatment ( n = 4 per group). m – p Flow cytometric analysis of antigen presentation and co-stimulatory molecules (CD14, ICAM-1, MHC-I, and CD86) on neutrophils cultured with tumor-conditioned medium derived from control, LDRT-, or HDRT-treated tumors ( n = 10 per group). Tumor growth curves ( q , r ) and survival curve ( s ) of LLC-bearing mice treated with TRIDENT alone or with GM-CSF/IFN-γ blockade ( n = 6 per group). Data are mean ± SEM. Statistical significance was assessed by one-way ANOVA ( b, f, g, k – p ), Student’s t test ( d ), two-way ANOVA ( h , i, q , r ) or log-rank test for survival ( j , s ). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001
2 1 2 Cxcr2 Pharmacological Inhibition Mice, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Eurofins cho k1 cxcr2
Evaluation of functional differences between IL-8 and CXCL1 in neutrophils. ( A ) Evaluation of IL-8 and CXCL1 activity in the U2OS-CXCR1 reporter cells ( left <t>)</t> <t>and</t> <t>CHO-K1-CXCR2</t> reporter cells ( right ). ( B ) Flow cytometric analysis of CXCR1 and CXCR2 surface expression on neutrophils. ( C ) Neutrophil chemotaxis assay toward IL-8 or CXCL1. RLU, relative luminescence units. Data in ( A ) and ( C ) are presented as the mean ± SD (n = 3).
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TRIDENT induces chemotactic and polarizing signals that recruit and program neutrophils toward an antitumor phenotype. a Schematic of the in vitro Transwell assay evaluating neutrophil migration toward tumor-conditioned medium derived from the indicated treatments. b Quantification of neutrophil migration across Transwell membranes ( n = 4 per group). c Experimental design of the in vivo neutrophil-trafficking assay in a dual-tumor model after indicated therapy. d Representative flow cytometry plots and quantification of transferred CD45.1⁺ neutrophils in tumors ( n = 7 per group). e Single-cell RNA-seq showing Cxcr2 upregulation in neutrophils from TRIDENT-treated tumors. Genes were classified as upregulated if increased in both comparisons, downregulated if decreased in both, oppositely regulated if significant in both but with opposite direction, and unchanged if non-significant in ≥1 comparison or showed minimal change. f Flow cytometric quantification of CXCR2⁺ neutrophils in second tumors in the LLC model across treatment groups ( n = 7 per group). g Heatmap comparing relative mRNA expression of Cxcl1, Cxcl2, Cxcl3 , and Cxcl5 from averaged qPCR values in tumor tissues after the indicated treatment ( n = 4 per group). Tumor growth curves ( h , i ) and survival curve ( j ) of LLC-bearing mice treated with TRIDENT alone or with CXCR2 blockade ( n = 9 per group). k, l qPCR analysis showing increased expression of Csf2 and Ifng in tumor tissues after indicated treatment ( n = 4 per group). m – p Flow cytometric analysis of antigen presentation and co-stimulatory molecules (CD14, ICAM-1, MHC-I, and CD86) on neutrophils cultured with tumor-conditioned medium derived from control, LDRT-, or HDRT-treated tumors ( n = 10 per group). Tumor growth curves ( q , r ) and survival curve ( s ) of LLC-bearing mice treated with TRIDENT alone or with GM-CSF/IFN-γ blockade ( n = 6 per group). Data are mean ± SEM. Statistical significance was assessed by one-way ANOVA ( b, f, g, k – p ), Student’s t test ( d ), two-way ANOVA ( h , i, q , r ) or log-rank test for survival ( j , s ). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001

Journal: Signal Transduction and Targeted Therapy

Article Title: Low-dose radiotherapy synergizes with PD-1 blockade to achieve durable survival in advanced NSCLC through antitumor neutrophil programming

doi: 10.1038/s41392-026-02712-6

Figure Lengend Snippet: TRIDENT induces chemotactic and polarizing signals that recruit and program neutrophils toward an antitumor phenotype. a Schematic of the in vitro Transwell assay evaluating neutrophil migration toward tumor-conditioned medium derived from the indicated treatments. b Quantification of neutrophil migration across Transwell membranes ( n = 4 per group). c Experimental design of the in vivo neutrophil-trafficking assay in a dual-tumor model after indicated therapy. d Representative flow cytometry plots and quantification of transferred CD45.1⁺ neutrophils in tumors ( n = 7 per group). e Single-cell RNA-seq showing Cxcr2 upregulation in neutrophils from TRIDENT-treated tumors. Genes were classified as upregulated if increased in both comparisons, downregulated if decreased in both, oppositely regulated if significant in both but with opposite direction, and unchanged if non-significant in ≥1 comparison or showed minimal change. f Flow cytometric quantification of CXCR2⁺ neutrophils in second tumors in the LLC model across treatment groups ( n = 7 per group). g Heatmap comparing relative mRNA expression of Cxcl1, Cxcl2, Cxcl3 , and Cxcl5 from averaged qPCR values in tumor tissues after the indicated treatment ( n = 4 per group). Tumor growth curves ( h , i ) and survival curve ( j ) of LLC-bearing mice treated with TRIDENT alone or with CXCR2 blockade ( n = 9 per group). k, l qPCR analysis showing increased expression of Csf2 and Ifng in tumor tissues after indicated treatment ( n = 4 per group). m – p Flow cytometric analysis of antigen presentation and co-stimulatory molecules (CD14, ICAM-1, MHC-I, and CD86) on neutrophils cultured with tumor-conditioned medium derived from control, LDRT-, or HDRT-treated tumors ( n = 10 per group). Tumor growth curves ( q , r ) and survival curve ( s ) of LLC-bearing mice treated with TRIDENT alone or with GM-CSF/IFN-γ blockade ( n = 6 per group). Data are mean ± SEM. Statistical significance was assessed by one-way ANOVA ( b, f, g, k – p ), Student’s t test ( d ), two-way ANOVA ( h , i, q , r ) or log-rank test for survival ( j , s ). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001

Article Snippet: For CXCR2 blockade, a CXCR2 antagonist (HY-101022, MedChemExpress; 2 mg/kg, i.p.) was administered every 3 days from randomization.

Techniques: In Vitro, Transwell Assay, Migration, Derivative Assay, In Vivo, Flow Cytometry, Single Cell, RNA Sequencing, Comparison, Expressing, Immunopeptidomics, Cell Culture, Control

TRIDENT induces chemotactic and polarizing signals that recruit and program neutrophils toward an antitumor phenotype. a Schematic of the in vitro Transwell assay evaluating neutrophil migration toward tumor-conditioned medium derived from the indicated treatments. b Quantification of neutrophil migration across Transwell membranes ( n = 4 per group). c Experimental design of the in vivo neutrophil-trafficking assay in a dual-tumor model after indicated therapy. d Representative flow cytometry plots and quantification of transferred CD45.1⁺ neutrophils in tumors ( n = 7 per group). e Single-cell RNA-seq showing Cxcr2 upregulation in neutrophils from TRIDENT-treated tumors. Genes were classified as upregulated if increased in both comparisons, downregulated if decreased in both, oppositely regulated if significant in both but with opposite direction, and unchanged if non-significant in ≥1 comparison or showed minimal change. f Flow cytometric quantification of CXCR2⁺ neutrophils in second tumors in the LLC model across treatment groups ( n = 7 per group). g Heatmap comparing relative mRNA expression of Cxcl1, Cxcl2, Cxcl3 , and Cxcl5 from averaged qPCR values in tumor tissues after the indicated treatment ( n = 4 per group). Tumor growth curves ( h , i ) and survival curve ( j ) of LLC-bearing mice treated with TRIDENT alone or with CXCR2 blockade ( n = 9 per group). k, l qPCR analysis showing increased expression of Csf2 and Ifng in tumor tissues after indicated treatment ( n = 4 per group). m – p Flow cytometric analysis of antigen presentation and co-stimulatory molecules (CD14, ICAM-1, MHC-I, and CD86) on neutrophils cultured with tumor-conditioned medium derived from control, LDRT-, or HDRT-treated tumors ( n = 10 per group). Tumor growth curves ( q , r ) and survival curve ( s ) of LLC-bearing mice treated with TRIDENT alone or with GM-CSF/IFN-γ blockade ( n = 6 per group). Data are mean ± SEM. Statistical significance was assessed by one-way ANOVA ( b, f, g, k – p ), Student’s t test ( d ), two-way ANOVA ( h , i, q , r ) or log-rank test for survival ( j , s ). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001

Journal: Signal Transduction and Targeted Therapy

Article Title: Low-dose radiotherapy synergizes with PD-1 blockade to achieve durable survival in advanced NSCLC through antitumor neutrophil programming

doi: 10.1038/s41392-026-02712-6

Figure Lengend Snippet: TRIDENT induces chemotactic and polarizing signals that recruit and program neutrophils toward an antitumor phenotype. a Schematic of the in vitro Transwell assay evaluating neutrophil migration toward tumor-conditioned medium derived from the indicated treatments. b Quantification of neutrophil migration across Transwell membranes ( n = 4 per group). c Experimental design of the in vivo neutrophil-trafficking assay in a dual-tumor model after indicated therapy. d Representative flow cytometry plots and quantification of transferred CD45.1⁺ neutrophils in tumors ( n = 7 per group). e Single-cell RNA-seq showing Cxcr2 upregulation in neutrophils from TRIDENT-treated tumors. Genes were classified as upregulated if increased in both comparisons, downregulated if decreased in both, oppositely regulated if significant in both but with opposite direction, and unchanged if non-significant in ≥1 comparison or showed minimal change. f Flow cytometric quantification of CXCR2⁺ neutrophils in second tumors in the LLC model across treatment groups ( n = 7 per group). g Heatmap comparing relative mRNA expression of Cxcl1, Cxcl2, Cxcl3 , and Cxcl5 from averaged qPCR values in tumor tissues after the indicated treatment ( n = 4 per group). Tumor growth curves ( h , i ) and survival curve ( j ) of LLC-bearing mice treated with TRIDENT alone or with CXCR2 blockade ( n = 9 per group). k, l qPCR analysis showing increased expression of Csf2 and Ifng in tumor tissues after indicated treatment ( n = 4 per group). m – p Flow cytometric analysis of antigen presentation and co-stimulatory molecules (CD14, ICAM-1, MHC-I, and CD86) on neutrophils cultured with tumor-conditioned medium derived from control, LDRT-, or HDRT-treated tumors ( n = 10 per group). Tumor growth curves ( q , r ) and survival curve ( s ) of LLC-bearing mice treated with TRIDENT alone or with GM-CSF/IFN-γ blockade ( n = 6 per group). Data are mean ± SEM. Statistical significance was assessed by one-way ANOVA ( b, f, g, k – p ), Student’s t test ( d ), two-way ANOVA ( h , i, q , r ) or log-rank test for survival ( j , s ). *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001

Article Snippet: For CXCR2 blockade, a CXCR2 antagonist (HY-101022, MedChemExpress; 2 mg/kg, i.p.) was administered every 3 days from randomization.

Techniques: In Vitro, Transwell Assay, Migration, Derivative Assay, In Vivo, Flow Cytometry, Single Cell, RNA Sequencing, Comparison, Expressing, Immunopeptidomics, Cell Culture, Control

Evaluation of functional differences between IL-8 and CXCL1 in neutrophils. ( A ) Evaluation of IL-8 and CXCL1 activity in the U2OS-CXCR1 reporter cells ( left ) and CHO-K1-CXCR2 reporter cells ( right ). ( B ) Flow cytometric analysis of CXCR1 and CXCR2 surface expression on neutrophils. ( C ) Neutrophil chemotaxis assay toward IL-8 or CXCL1. RLU, relative luminescence units. Data in ( A ) and ( C ) are presented as the mean ± SD (n = 3).

Journal: Scientific Reports

Article Title: IL-8 contributes to postoperative adhesion formation through the crosstalk of neutrophils and mesothelial cells

doi: 10.1038/s41598-026-42159-x

Figure Lengend Snippet: Evaluation of functional differences between IL-8 and CXCL1 in neutrophils. ( A ) Evaluation of IL-8 and CXCL1 activity in the U2OS-CXCR1 reporter cells ( left ) and CHO-K1-CXCR2 reporter cells ( right ). ( B ) Flow cytometric analysis of CXCR1 and CXCR2 surface expression on neutrophils. ( C ) Neutrophil chemotaxis assay toward IL-8 or CXCL1. RLU, relative luminescence units. Data in ( A ) and ( C ) are presented as the mean ± SD (n = 3).

Article Snippet: CHO-K1-CXCR2 were maintained in AssayCompleteTM Cell Culture Kit-107 (Eurofins DiscoverX).

Techniques: Functional Assay, Activity Assay, Expressing, Chemotaxis Assay