Journal: British Journal of Cancer

Article Title: Early expression of the fractalkine receptor CX3CR1 in pancreatic carcinogenesis

doi: 10.1038/bjc.2013.565

Figure Lengend Snippet: CX3CR1 and CX3CL1 expression in normal pancreas and in pancreatic cancer. ( A ) CX3CR1 expression in normal pancreas, ( B ) in well- and ( C ) in poorly differentiated PDAC, and ( B , inset) in inflammatory cells in tumour microenvironment. ( D ) CX3CL1 expression in normal pancreas, ( E ) in neural cell bodies, and ( F ) in PDAC (box, × 40 magnification of a CX3CL1 + PDAC). Objective magnification × 10 ( A – D and F ); ( E ) and inset in ( B ), × 40. ( G ) Frequency of CX3CR1 + and CX3CR1 − PDAC with PNI according to tumour differentiation (Grade, G1–G2 well-to-moderately differentiated PDAC; G3, poorly differentiated PDAC). ( H ) Kaplan–Meier curves for overall survival of patients after radical resection of PDAC ( n =67), according to the status of CX3-CR1 (left panel) and -CL1 (right panel) in cancer. P -values by log-rank test. * indicates P <0.05.

Article Snippet: After deparaffining and rehydration, the sections were immersed in antigen retrieval bath, incubated with 3% H 2 O 2 for 15 min, and treated for 2 h at room temperature with primary antibodies raised against CX3CR1 (Ab8021, polyclonal rabbit anti-human; Abcam, Cambridge, UK) and CX3CL1 (AF365, polyclonal goat anti-human; R&D Systems, Minneapolis, MN, USA), or with rabbit or goat IgG (Dako, Milan, Italy) to serve as negative controls, followed by 30-min incubation with the DAKO Envision system (Dako) or the Anti-Goat Polymer kit (Biocare, San Francisco, CA, USA).

Techniques: Expressing

Journal: British Journal of Cancer

Article Title: Early expression of the fractalkine receptor CX3CR1 in pancreatic carcinogenesis

doi: 10.1038/bjc.2013.565

Figure Lengend Snippet: CX3CR1 and CX3CL1 expression in 104 PDAC according to patients' demographics and to tumour features

Article Snippet: After deparaffining and rehydration, the sections were immersed in antigen retrieval bath, incubated with 3% H 2 O 2 for 15 min, and treated for 2 h at room temperature with primary antibodies raised against CX3CR1 (Ab8021, polyclonal rabbit anti-human; Abcam, Cambridge, UK) and CX3CL1 (AF365, polyclonal goat anti-human; R&D Systems, Minneapolis, MN, USA), or with rabbit or goat IgG (Dako, Milan, Italy) to serve as negative controls, followed by 30-min incubation with the DAKO Envision system (Dako) or the Anti-Goat Polymer kit (Biocare, San Francisco, CA, USA).

Techniques: Expressing

Journal: British Journal of Cancer

Article Title: Early expression of the fractalkine receptor CX3CR1 in pancreatic carcinogenesis

doi: 10.1038/bjc.2013.565

Figure Lengend Snippet: Tumour differentiation, peri-neural invasion, and ligand expression are independently associated with CX3CR1 expression

Article Snippet: After deparaffining and rehydration, the sections were immersed in antigen retrieval bath, incubated with 3% H 2 O 2 for 15 min, and treated for 2 h at room temperature with primary antibodies raised against CX3CR1 (Ab8021, polyclonal rabbit anti-human; Abcam, Cambridge, UK) and CX3CL1 (AF365, polyclonal goat anti-human; R&D Systems, Minneapolis, MN, USA), or with rabbit or goat IgG (Dako, Milan, Italy) to serve as negative controls, followed by 30-min incubation with the DAKO Envision system (Dako) or the Anti-Goat Polymer kit (Biocare, San Francisco, CA, USA).

Techniques: Expressing

Journal: British Journal of Cancer

Article Title: Early expression of the fractalkine receptor CX3CR1 in pancreatic carcinogenesis

doi: 10.1038/bjc.2013.565

Figure Lengend Snippet: Expression of CX3CR1 and CX3CL1 in precursor lesions according to tumour differentiation and PanIN degree. ( A ) Comparison of the expression rate of CX3CR1 (upper panels) and CX3CL1 (lower panels) in paired precursor lesions and invasive cancers within the same tissue specimens ( n =76), according to the degree of pancreatic cancer differentiation. Number within bars, number of specimens. ( B ) Rates of CX3CR1 + (upper panels) and CX3CL1 + (lower panels) PanINs according to their degree of dysplasia. Numbers within bars, number of PanINs. G1–G2 tumours, left panels; G3 tumours, right panels; P -values by Fisher's exact test.

Article Snippet: After deparaffining and rehydration, the sections were immersed in antigen retrieval bath, incubated with 3% H 2 O 2 for 15 min, and treated for 2 h at room temperature with primary antibodies raised against CX3CR1 (Ab8021, polyclonal rabbit anti-human; Abcam, Cambridge, UK) and CX3CL1 (AF365, polyclonal goat anti-human; R&D Systems, Minneapolis, MN, USA), or with rabbit or goat IgG (Dako, Milan, Italy) to serve as negative controls, followed by 30-min incubation with the DAKO Envision system (Dako) or the Anti-Goat Polymer kit (Biocare, San Francisco, CA, USA).

Techniques: Expressing, Comparison

Journal: British Journal of Cancer

Article Title: Early expression of the fractalkine receptor CX3CR1 in pancreatic carcinogenesis

doi: 10.1038/bjc.2013.565

Figure Lengend Snippet: CX3CR1 and CX3CL1 expression in precursor lesions of pancreatic cancer. ( A ) Left panels, human PanINs; right panels, PanINs of PdxCre/LSL- Kras G12D mice. Objective magnification, × 20 (human PanINs), and × 40 (mice PanINs). ( B ) Precursor lesions adjacent to neural structures. Detection of precursor lesions close to (left panel) or in tight contact with (right panel) S-100 + neural structures (red arrows) in pancreata of 6-month-old PdxCre/LSL-Kras G12D mice. Magnification, × 20.

Article Snippet: After deparaffining and rehydration, the sections were immersed in antigen retrieval bath, incubated with 3% H 2 O 2 for 15 min, and treated for 2 h at room temperature with primary antibodies raised against CX3CR1 (Ab8021, polyclonal rabbit anti-human; Abcam, Cambridge, UK) and CX3CL1 (AF365, polyclonal goat anti-human; R&D Systems, Minneapolis, MN, USA), or with rabbit or goat IgG (Dako, Milan, Italy) to serve as negative controls, followed by 30-min incubation with the DAKO Envision system (Dako) or the Anti-Goat Polymer kit (Biocare, San Francisco, CA, USA).

Techniques: Expressing

Journal: British Journal of Cancer

Article Title: Early expression of the fractalkine receptor CX3CR1 in pancreatic carcinogenesis

doi: 10.1038/bjc.2013.565

Figure Lengend Snippet: Effects of microenvironmental stimuli on CX3CR1 and CX3CL1 expression in pancreatic tumoral cells. CX3CR1 (left panels) and CX3CL1 (right panels) mRNA fold changes induced by stimulation with TNF- α +IFN- γ , IL-1 β , IL-6, and by TGF- β in mouse DT6606 ( PdxCre/LSL-Kras G12 model) and K8484 ( PdxCre/LSL - Kras G12D - Trp53 R172H model) cells, and in human A8184, AspCI, and MiaPacaII pancreatic cancer cells. * indicates P <0.05.

Article Snippet: After deparaffining and rehydration, the sections were immersed in antigen retrieval bath, incubated with 3% H 2 O 2 for 15 min, and treated for 2 h at room temperature with primary antibodies raised against CX3CR1 (Ab8021, polyclonal rabbit anti-human; Abcam, Cambridge, UK) and CX3CL1 (AF365, polyclonal goat anti-human; R&D Systems, Minneapolis, MN, USA), or with rabbit or goat IgG (Dako, Milan, Italy) to serve as negative controls, followed by 30-min incubation with the DAKO Envision system (Dako) or the Anti-Goat Polymer kit (Biocare, San Francisco, CA, USA).

Techniques: Expressing

Journal: bioRxiv

Article Title: A CD40-Targeted IL-21 Fusokine Enables Rapid Generation of Human IL-10⁺Granzyme B⁺ Regulatory B Cells

doi: 10.64898/2026.01.12.699061

Figure Lengend Snippet: (A) Principal component analysis (PCA) of RNA-seq data from purified human peripheral blood B cells cultured under four conditions: unstimulated B cells, CpG-stimulated B cells (B-CpG), CD40scFv–IL-21–stimulated B cells (B-ScFv), and B cells stimulated with the combination of CD40scFv–IL-21 and CpG (Bregs). PCA demonstrates clear separation among conditions, indicating distinct global transcriptional states induced by single versus combined stimulation. (B) Venn diagram showing the number of genes upregulated (log₂ fold change > 1) relative to unstimulated B cells in B-CpG, B-ScFv, and Bregs. The overlap highlights both shared and condition-specific transcriptional responses, with Bregs exhibiting a distinct set of upregulated genes not observed with single-stimulus activation. (C) Volcano plot depicting differential gene expression between Bregs and B-CpG cells. The x-axis represents log₂ fold change (Bregs vs B-CpG), and the y-axis represents −log₁₀ adjusted p-value. Genes significantly upregulated in Bregs include regulatory and effector-associated transcripts such as IL10, GZMB, CD274 (PD-L1), PDCD1LG2 (PD-L2) , and EBI3 , whereas CpG-associated inflammatory and chemokine-related genes are less prominent under combined stimulation. (D) Heat map showing expression of selected regulatory, checkpoint, transcriptional, and chemokine-associated genes comparing B-CpG and Bregs across three independent donors (D312, D919, D936). Expression values are displayed as log₂(FPKM + 1) and visualized using a red–blue diverging color scale, with red indicating higher relative expression and blue indicating lower expression. The heat map reveals coordinated upregulation of regulatory and effector-associated genes ( IL10, GZMB, CD274, PDCD1LG2, EBI3, PRDM1, IRF4 ) in Bregs, whereas B-CpG cells show relatively higher expression of chemokines such as CCL3 and CCL4 .

Article Snippet: Chemokine expression was assessed using the Proteome Profiler Human Chemokine Array Kit (R&D Systems, ARY017) according to the manufacturer’s instructions.

Techniques: RNA Sequencing, Purification, Cell Culture, Activation Assay, Gene Expression, Expressing

Journal: Scientific Reports

Article Title: Chronic inflammation promotes gastric cancer progression via ADAM10-mediated cleavage of CX3CL1

doi: 10.1038/s41598-026-39743-6

Figure Lengend Snippet: High CX3CL1 enrichment in the CI group predicts poor prognosis of GC patients. ( A ) Schematic of detecting cytokines in mouse serum via cytokine array. ( B ) Volcano plots depicting the differential analysis of detected cytokines in CI and CON( n = 3 per group). ( C ) Schematic of screening differentially expressed cytokines between CI and CON groups by P value and log 2 (FC). ( D , E , F ) Survival curves for GC patients with low or high expression of MMP2/COL18A1/CX3CL1 in GEO database using Kaplan-Meier method. ( G ) The mRNA level of CX3CL1 in GC tissues compared with normal tissues in TCGA-STAD datasets. ( H ) The mRNA level of CX3CL1 in GC tissues between different T-stage from TCGA-STAD datasets. ( I ) Survival curves for GC patients with low or high expression of CX3CL1 in TCGA database using Kaplan-Meier method. ( J ) Concentration of CX3CL1 in the mice tumors detected by ELISA( n = 3 per group). Data are represented as mean ± SEM. * P < 0.05,** P < 0.01,*** P < 0.001(J: two-tailed unpaired Student’s t test).

Article Snippet: The concentrations of CX3CL1 in the tumor tissue were quantified using commercially CX3CL1 ELISA kit (Proteintech, KE10076) according to the kit instructions.

Techniques: Expressing, Concentration Assay, Enzyme-linked Immunosorbent Assay, Two Tailed Test

Journal: Scientific Reports

Article Title: Chronic inflammation promotes gastric cancer progression via ADAM10-mediated cleavage of CX3CL1

doi: 10.1038/s41598-026-39743-6

Figure Lengend Snippet: Single-cell transcriptomic characterization of CX3CL1 expression. ( A ) Dimensionality reduction and sample visualization analysis of tSNE. ( B ) Manual annotation of cell types based on Marker gene annotation. ( C ) tSNE plots of scRNA-seq from CON and CI groups. ( D ) Inflammation score mapping illustrating differences in the cellular distribution of inflammatory transcriptional signatures between CON and CI tumors. ( E ) Violin plot showing the distribution of Cx3cl1 expression across annotated cell types. ( F ) Feature plot visualization of Cx3cl1 expression on the t-SNE map in CON and CI groups. ( G ) Violin plot showing the distribution of Cx3cr1 expression across annotated cell types. ( H ) Feature plot visualization of Cx3cr1 expression on the t-SNE map in CON and CI groups. ( I ) GO enrichment analysis. ( J ) KEGG enrichment analysis of differentially expressed genes comparing the Tumor_6 subcluster with other tumor cell subclusters. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Article Snippet: The concentrations of CX3CL1 in the tumor tissue were quantified using commercially CX3CL1 ELISA kit (Proteintech, KE10076) according to the kit instructions.

Techniques: Single Cell, Expressing, Marker

Journal: Scientific Reports

Article Title: Chronic inflammation promotes gastric cancer progression via ADAM10-mediated cleavage of CX3CL1

doi: 10.1038/s41598-026-39743-6

Figure Lengend Snippet: CX3CL1 promotes gastric cancer cell proliferation and migration via CX3CR1. ( A , B ) Relative mRNA expression levels of CX3CR1/Cx3cr1 in GES-1, HGC-27, RAW264.7 and MFC cells. ( C ) Protein expression of CX3CR1 in GES-1, HGC-27, RAW264.7, and MFC cells. ( D , E ) Cell viability of MFC ( D ) and HGC-27 ( E ) cells treated with increasing concentrations of CX3CL1 ( n = 3 per group). ( F , G ) Representative images ( F ) and quantification ( G ) of colony formation assays in MFC and HGC-27 cells treated with CX3CL1( n = 3 per group). ( H , I ) Representative images ( H ) and quantification ( I ) of Transwell migration assays in MFC and HGC-27 cells treated with CX3CL1 ( n = 3 per group). Scale bar, 50 μm. ( J , K ) Representative images ( J ) and quantification ( K ) of wound-healing assays in MFC and HGC-27 cells treated with CX3CL1 for 24 h ( n = 3 per group). Scale bar, 500 μm. ( L - P ) The effects of CX3CL1 on cell viability ( L ), wound-healing migration ( N ), and Transwell migration ( O , P ) were further examined in the presence or absence of the CX3CR1 inhibitor JMS-17-2. Data are presented as mean ± SEM from independent experiments. For panels D and E, statistical significance is indicated relative to the 0 ng/mL CX3CL1 group. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001; ns, not significant. ( D , E ) one-way ANOVA with Dunnett’s multiple comparisons test; ( F - K ) two-tailed unpaired Student’s t-test; (L - P) two-way ANOVA with Sidak’s multiple comparisons test(interaction P = 0.0034, 0.0079, 0.0033, 0.0163, 0.0156, and 0.0311 for panels L - P , respectively).

Article Snippet: The concentrations of CX3CL1 in the tumor tissue were quantified using commercially CX3CL1 ELISA kit (Proteintech, KE10076) according to the kit instructions.

Techniques: Migration, Expressing, Two Tailed Test

Journal: Scientific Reports

Article Title: Chronic inflammation promotes gastric cancer progression via ADAM10-mediated cleavage of CX3CL1

doi: 10.1038/s41598-026-39743-6

Figure Lengend Snippet: ADAM10-mediated increased cleavage of CX3CL1 contributes to CI-promoted GC progression. ( A-C ) RT-qPCR and Western blot confirmed that CI increased the mRNA and protein expression of ADAM10 in tumor tissues( n = 3 per group). ( D ) Immunofluorescence assay suggested the increase of ADAM10 (Red) fluorescence intensity in tumor tissues. ( E-F ) Western blot confirmed that LPS increased the protein expression of ADAM10 in GC cell lines( n = 3 per group). ( G ) ELISA assay demonstrated that the ADAM10 antagonist GI254023X could attenuate the LPS-induced increase in soluble CX3CL1 levels in GC cells( n = 3 per group). ( H-N ) ADAM10 antagonist GI254023X inhibited LPS-promoted GC cells migration and invasion( n = 3 per group). ( O ) Schematic diagram shows the experimental protocol for determine the effect of ADAM10 inhibitor GI in suppressingsing CI-promoted tumor progression in mice( n = 5 per group). ( P-Q ) Left: Representative macroscopic images of tumors; Right: weight of tumors( n = 5 per group). ( R ) Concentration of CX3CL1 in the mice tumors detected by ELISA( n = 3 per group). Data are represented as mean ± SEM. For panel F, statistical significance was determined relative to the 0 µg/mL LPS group. For panels G , I , K , N , statistical significance was determined relative to the LPS group. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001(A, C: two-tailed unpaired Student’s t test; F , G , I , K , N , Q , R : one-way ANOVA with Dunnett’s multiple comparisons test).

Article Snippet: The concentrations of CX3CL1 in the tumor tissue were quantified using commercially CX3CL1 ELISA kit (Proteintech, KE10076) according to the kit instructions.

Techniques: Quantitative RT-PCR, Western Blot, Expressing, Immunofluorescence, Fluorescence, Enzyme-linked Immunosorbent Assay, Migration, Concentration Assay, Two Tailed Test

Journal: Scientific Reports

Article Title: Chronic inflammation promotes gastric cancer progression via ADAM10-mediated cleavage of CX3CL1

doi: 10.1038/s41598-026-39743-6

Figure Lengend Snippet: Graphical Abstract. CI induces the upregulation of ADAM10 expression in GC cells. Upregulated ADAM10 mediates the cleavage of membrane-bound CX3CL1 (mCX3CL1), thereby promoting the release of soluble CX3CL1 (sCX3CL1). The increased sCX3CL1 ultimately enhance GC cell proliferation and migration to accelerate tumor progression.

Article Snippet: The concentrations of CX3CL1 in the tumor tissue were quantified using commercially CX3CL1 ELISA kit (Proteintech, KE10076) according to the kit instructions.

Techniques: Expressing, Membrane, Migration