recombinant human cx3cl1/fractalkine (full length) protein  (Bio-Techne corporation)

Journal: Signal Transduction and Targeted Therapy

Article Title: Synergistic immunotherapeutic effects of irreversible electroporation and CAR-NK cell therapy against hepatocellular carcinoma

doi: 10.1038/s41392-026-02627-2

Figure Lengend Snippet: PEF exposure to liver cancer cells induces the recruitment of NK cells via CX3CL1 chemotaxis. a Representative images from live cell analysis of Hepa1c1c7 and Huh-7 cells after 24 h of PEF exposure. The red and yellow areas indicate the ablation zone. b ATP release from Hepa1c1c7 and Huh-7 cells after 2 h of PEF exposure. c HMGB1 released from Hepa1c1c7 and Huh-7 cells after 24 h of PEF exposure d (Left) Representative flow cytometric histogram and (right) quantified bar graph of calreticulin-presented Hepa1c1c7 and Huh-7 cells after 24 h of PEF exposure. e Migration analysis of CFSE-labeled NK92MI and f mouse primary NK cells (mNK) toward conditioned medium (CM) from PEF-exposed liver cancer cell lines (PEF-CM). Scale bar = 100 μm and 50 μm, respectively. g Concentration of CX3CL1 in PEF-CM from Hepa1c1c7 and Huh-7 cells. h Concentration of CX3CL1 at the indicated time points after IRE treatment in orthotopic Hepa1c1c7 tumors in C57BL/6 mice. i Migration analysis of CFSE-labeled NK92MI cells toward PEF-CM, including CX3CL1-neutralizing antibody. Scale bar = 100 μm. j Caspase-3/7 activation in PEF-exposed Huh-7 cells cocultured with migrated NK92MI cells. Scale bar = 50 μm. k Scheme of PEF-mediated CX3CL1 release and NK cell recruitment. Data represent the mean ± S.D. ( n = 3; biological replicates). A two-tailed Student’s t test was used for the P value ( b – j ). Panels e , f , j , and k were created with BioRender.com

Article Snippet: To determine the levels of human CX3CL1 and mouse CX3CL1 in PEF-CM from Huh-7 and Hepa1c1c7 cells, ELISA was performed using reagents from ABclonal Biotechnology.

Techniques: Chemotaxis Assay, Cell Analysis, Migration, Labeling, Concentration Assay, Activation 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: 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