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quantikine elisa  (R&D Systems)


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    Structured Review

    R&D Systems quantikine elisa
    IL-1β stimulation increases expression of neutrophil recruitment and NF-kB signaling genes by BM-hMSCs. Heatmap clustering of the Z-score of the top 20 differentially expressed genes between unstimulated control BM-hMSCs (3 replicates, 1 donor, green) and IL-1 β stimulated BM-hMSCs (3 replicates, 1 donor, purple). Red color indicates higher expression of the genes and blue color indicates decreased expression A . Protein expression of CXCL1 (10 replicates, 4 donors), CCL2 (4 replicates, 2 donors), CXCL5 (4 replicates, 2 donors), and CXCL8/IL-8 (7 replicates, 3 donors) in BM-hMSCs secretome measured by ELLA or <t>ELISA.</t> Data are presented as median, and statistical analysis was performed using unpaired t-test with Welch’s correction B . Bar plot of the top 20 significant Gene Ontology (GO) biological processes representing IL- 1β induced upregulated differentially expressed genes C IL-1 β, Interleukin-1β; BM-hMSCs, Bone marrow derived human mesenchymal cells; CCL2, chemokine (C–C motif) ligand 2; CXCL1, chemokine (C-X-C motif) ligand 1; CXCL2, chemokine (C-X-C motif) ligand 1; CXCL8, chemokine (C-X-C motif) ligand 8; ****, p < 0,0001
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    Images

    1) Product Images from "IL-1β modulates inflammatory response of human bone marrow-derived MSCs and neutrophil recruitment in vitro via NF-kB-associated signaling"

    Article Title: IL-1β modulates inflammatory response of human bone marrow-derived MSCs and neutrophil recruitment in vitro via NF-kB-associated signaling

    Journal: Stem Cell Research & Therapy

    doi: 10.1186/s13287-026-05029-x

    IL-1β stimulation increases expression of neutrophil recruitment and NF-kB signaling genes by BM-hMSCs. Heatmap clustering of the Z-score of the top 20 differentially expressed genes between unstimulated control BM-hMSCs (3 replicates, 1 donor, green) and IL-1 β stimulated BM-hMSCs (3 replicates, 1 donor, purple). Red color indicates higher expression of the genes and blue color indicates decreased expression A . Protein expression of CXCL1 (10 replicates, 4 donors), CCL2 (4 replicates, 2 donors), CXCL5 (4 replicates, 2 donors), and CXCL8/IL-8 (7 replicates, 3 donors) in BM-hMSCs secretome measured by ELLA or ELISA. Data are presented as median, and statistical analysis was performed using unpaired t-test with Welch’s correction B . Bar plot of the top 20 significant Gene Ontology (GO) biological processes representing IL- 1β induced upregulated differentially expressed genes C IL-1 β, Interleukin-1β; BM-hMSCs, Bone marrow derived human mesenchymal cells; CCL2, chemokine (C–C motif) ligand 2; CXCL1, chemokine (C-X-C motif) ligand 1; CXCL2, chemokine (C-X-C motif) ligand 1; CXCL8, chemokine (C-X-C motif) ligand 8; ****, p < 0,0001
    Figure Legend Snippet: IL-1β stimulation increases expression of neutrophil recruitment and NF-kB signaling genes by BM-hMSCs. Heatmap clustering of the Z-score of the top 20 differentially expressed genes between unstimulated control BM-hMSCs (3 replicates, 1 donor, green) and IL-1 β stimulated BM-hMSCs (3 replicates, 1 donor, purple). Red color indicates higher expression of the genes and blue color indicates decreased expression A . Protein expression of CXCL1 (10 replicates, 4 donors), CCL2 (4 replicates, 2 donors), CXCL5 (4 replicates, 2 donors), and CXCL8/IL-8 (7 replicates, 3 donors) in BM-hMSCs secretome measured by ELLA or ELISA. Data are presented as median, and statistical analysis was performed using unpaired t-test with Welch’s correction B . Bar plot of the top 20 significant Gene Ontology (GO) biological processes representing IL- 1β induced upregulated differentially expressed genes C IL-1 β, Interleukin-1β; BM-hMSCs, Bone marrow derived human mesenchymal cells; CCL2, chemokine (C–C motif) ligand 2; CXCL1, chemokine (C-X-C motif) ligand 1; CXCL2, chemokine (C-X-C motif) ligand 1; CXCL8, chemokine (C-X-C motif) ligand 8; ****, p < 0,0001

    Techniques Used: Expressing, Control, Enzyme-linked Immunosorbent Assay, Derivative Assay



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    IL-1β stimulation increases expression of neutrophil recruitment and NF-kB signaling genes by BM-hMSCs. Heatmap clustering of the Z-score of the top 20 differentially expressed genes between unstimulated control BM-hMSCs (3 replicates, 1 donor, green) and IL-1 β stimulated BM-hMSCs (3 replicates, 1 donor, purple). Red color indicates higher expression of the genes and blue color indicates decreased expression A . Protein expression of CXCL1 (10 replicates, 4 donors), CCL2 (4 replicates, 2 donors), CXCL5 (4 replicates, 2 donors), and CXCL8/IL-8 (7 replicates, 3 donors) in BM-hMSCs secretome measured by ELLA or <t>ELISA.</t> Data are presented as median, and statistical analysis was performed using unpaired t-test with Welch’s correction B . Bar plot of the top 20 significant Gene Ontology (GO) biological processes representing IL- 1β induced upregulated differentially expressed genes C IL-1 β, Interleukin-1β; BM-hMSCs, Bone marrow derived human mesenchymal cells; CCL2, chemokine (C–C motif) ligand 2; CXCL1, chemokine (C-X-C motif) ligand 1; CXCL2, chemokine (C-X-C motif) ligand 1; CXCL8, chemokine (C-X-C motif) ligand 8; ****, p < 0,0001
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    Increased expression of <t>CXCL1</t> mRNA levels is associated with the clinical characteristics of patients with RCC. (A) The expression profiles of CXCL1 mRNA in normal tissues compared with ccRCC or pRCC tissues. The different levels of expression of CXCL1 mRNA within (B) different clinical grades and (C) subtypes of ccRCC tissues. Expression levels of CXCL1 mRNA in the (D) GSE53757 and the (E) GSE40435 datasets. The different levels of expression of CXCL1 mRNA within different (F) clinical grades and (G) stages of ccRCC tissues. Analysis of the expression level of CXCL1 within the clinical (H) T-status, (I) N-status and (J) M-status categories in ccRCC tissues. (K-M) A prognostic assessment was performed among the various groups. **P<0.01 vs. normal; # P<0.01 vs. normal, grade 1 and 2; ▲ P<0.01 vs. normal and ccA subtype. CXCL1, CXC motif chemokine ligand 1; RCC, renal cell carcinoma; ccRCC, clear cell RCC; pRCC, papillary RCC; T, tumor; N, lymph node; M, metastasis; OS, overall survival; DSS, disease-specific survival; PFS, progression-free survival.
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    Image Search Results


    IL-1β stimulation increases expression of neutrophil recruitment and NF-kB signaling genes by BM-hMSCs. Heatmap clustering of the Z-score of the top 20 differentially expressed genes between unstimulated control BM-hMSCs (3 replicates, 1 donor, green) and IL-1 β stimulated BM-hMSCs (3 replicates, 1 donor, purple). Red color indicates higher expression of the genes and blue color indicates decreased expression A . Protein expression of CXCL1 (10 replicates, 4 donors), CCL2 (4 replicates, 2 donors), CXCL5 (4 replicates, 2 donors), and CXCL8/IL-8 (7 replicates, 3 donors) in BM-hMSCs secretome measured by ELLA or ELISA. Data are presented as median, and statistical analysis was performed using unpaired t-test with Welch’s correction B . Bar plot of the top 20 significant Gene Ontology (GO) biological processes representing IL- 1β induced upregulated differentially expressed genes C IL-1 β, Interleukin-1β; BM-hMSCs, Bone marrow derived human mesenchymal cells; CCL2, chemokine (C–C motif) ligand 2; CXCL1, chemokine (C-X-C motif) ligand 1; CXCL2, chemokine (C-X-C motif) ligand 1; CXCL8, chemokine (C-X-C motif) ligand 8; ****, p < 0,0001

    Journal: Stem Cell Research & Therapy

    Article Title: IL-1β modulates inflammatory response of human bone marrow-derived MSCs and neutrophil recruitment in vitro via NF-kB-associated signaling

    doi: 10.1186/s13287-026-05029-x

    Figure Lengend Snippet: IL-1β stimulation increases expression of neutrophil recruitment and NF-kB signaling genes by BM-hMSCs. Heatmap clustering of the Z-score of the top 20 differentially expressed genes between unstimulated control BM-hMSCs (3 replicates, 1 donor, green) and IL-1 β stimulated BM-hMSCs (3 replicates, 1 donor, purple). Red color indicates higher expression of the genes and blue color indicates decreased expression A . Protein expression of CXCL1 (10 replicates, 4 donors), CCL2 (4 replicates, 2 donors), CXCL5 (4 replicates, 2 donors), and CXCL8/IL-8 (7 replicates, 3 donors) in BM-hMSCs secretome measured by ELLA or ELISA. Data are presented as median, and statistical analysis was performed using unpaired t-test with Welch’s correction B . Bar plot of the top 20 significant Gene Ontology (GO) biological processes representing IL- 1β induced upregulated differentially expressed genes C IL-1 β, Interleukin-1β; BM-hMSCs, Bone marrow derived human mesenchymal cells; CCL2, chemokine (C–C motif) ligand 2; CXCL1, chemokine (C-X-C motif) ligand 1; CXCL2, chemokine (C-X-C motif) ligand 1; CXCL8, chemokine (C-X-C motif) ligand 8; ****, p < 0,0001

    Article Snippet: CXCL1 was measured in diluted 1:1 or undiluted CM samples using Quantikine ELISA (cat# DGR00B, R&D Systems).

    Techniques: Expressing, Control, Enzyme-linked Immunosorbent Assay, Derivative Assay

    ABT-263 decreases senescence and alters the SASP in UPCI:SCC040 and Cal33 cells. Cells were treated with 1 µM ABT-263 (Cal33) or 5 µM of ABT-263 (UPCI:SCC040) concomitantly with 6 Gy irradiation and analyzed on D4 or D6. ( A-B ) Gene expression of secreted factors measured by qRT-PCR and normalized to unirradiated DMSO controls. ( A ) UPCI:SCC040. ( B ) Cal33. ( C-D ) Secreted IL1A, IL1B, IL8 and CXCL1 protein levels were detected by ELISA on D4 and D6. Protein concentrations (pg/ml) were normalized to cell number. ( C ) UPCI:SCC040. ( D ) Cal33. ( E-F ) Relative CXCR2 gene expression shown as ΔCT values in ( E ) Cal33 and ( F ) UPCI:SCC040 cells. Values a represent means ± SEM of N = 2. Student’s t test: p < 0.05 (*), p < 0.01 (**), ns: not significant

    Journal: Radiation Oncology (London, England)

    Article Title: CXCR2 affects sensitization of radioresistant HPV-negative head and neck squamous cell carcinoma cells by ABT-263

    doi: 10.1186/s13014-026-02798-w

    Figure Lengend Snippet: ABT-263 decreases senescence and alters the SASP in UPCI:SCC040 and Cal33 cells. Cells were treated with 1 µM ABT-263 (Cal33) or 5 µM of ABT-263 (UPCI:SCC040) concomitantly with 6 Gy irradiation and analyzed on D4 or D6. ( A-B ) Gene expression of secreted factors measured by qRT-PCR and normalized to unirradiated DMSO controls. ( A ) UPCI:SCC040. ( B ) Cal33. ( C-D ) Secreted IL1A, IL1B, IL8 and CXCL1 protein levels were detected by ELISA on D4 and D6. Protein concentrations (pg/ml) were normalized to cell number. ( C ) UPCI:SCC040. ( D ) Cal33. ( E-F ) Relative CXCR2 gene expression shown as ΔCT values in ( E ) Cal33 and ( F ) UPCI:SCC040 cells. Values a represent means ± SEM of N = 2. Student’s t test: p < 0.05 (*), p < 0.01 (**), ns: not significant

    Article Snippet: Cytokines IL-1α, IL-1β, IL-8 and CXCL1 were measured using DuoSet ELISA kits (R&D Systems, IL-1α Cat#DY200, IL-1β Cat#DY201-05, IL8 Cat#30021151, CXCL1 Cat#DY 275) according to manufacturer instructions.

    Techniques: Irradiation, Gene Expression, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay

    Correlations between LL-37 and citLL-37-mediated increase in the mRNA abundance of COX-2 and chemokines. HBEC-3KT cells were stimulated with either (⬤) LL-37 or (🞅) citLL-37 (0.50 µM each). mRNA abundance of COX-2, IL-8, GROα and MIP-3α were examined in cell lysates using qRT-PCR after 4 h. Relative fold changes were calculated compared to unstimulated cells normalized to 1, using the ΔΔCt method after normalization with 18s RNA expression. Pearson’s correlation analysis was performed to determine the correlation between COX-2 and ( a ) IL-8, ( b ) GROα and ( c ) MIP-3α mRNA abundance (fold changes compared to unstimulated cells)

    Journal: Respiratory Research

    Article Title: LL-37 and citrullinated-LL-37 enhances oxylipins: citrullination attenuates LL-37-mediated COX-2-dependent chemokine response in human bronchial epithelial cells

    doi: 10.1186/s12931-026-03493-w

    Figure Lengend Snippet: Correlations between LL-37 and citLL-37-mediated increase in the mRNA abundance of COX-2 and chemokines. HBEC-3KT cells were stimulated with either (⬤) LL-37 or (🞅) citLL-37 (0.50 µM each). mRNA abundance of COX-2, IL-8, GROα and MIP-3α were examined in cell lysates using qRT-PCR after 4 h. Relative fold changes were calculated compared to unstimulated cells normalized to 1, using the ΔΔCt method after normalization with 18s RNA expression. Pearson’s correlation analysis was performed to determine the correlation between COX-2 and ( a ) IL-8, ( b ) GROα and ( c ) MIP-3α mRNA abundance (fold changes compared to unstimulated cells)

    Article Snippet: The abundance of IL-8 (Cat# DY208), GROα (Cat# DY275) and MIP-3α (Cat# DY360) were examined in TC supernatants using ELISA kits obtained from R&D Systems, according to the manufacturer’s instructions.

    Techniques: Quantitative RT-PCR, RNA Expression

    Inhibition of COX-2 suppresses LL-37-mediated chemokine production. HBEC-3KT cells were pre-treated with COX-2 inhibitor Rofecoxib (20 nM) for 1 h, followed by stimulation with either LL-37, citLL-37 or sLL-37 (0.50 µM each) for 24 h (n = 5). TC supernatants were examined for the abundance of ( a ) IL-8, ( b ) GROα and ( c ) MIP-3α by ELISA. Chemokine levels shown in pg/mL after background subtraction of levels in unstimulated cells. Each dot represents an independent experiment (n = 5), the bars show IQR with the median line and the whiskers represent the min-max range. Statistical significance was measured using Two-Way ANOVA, and # represents statistical significance compared to unstimulated cells ( ** p < 0.005, *** p < 0.0005, #### or **** p < 0.0001)

    Journal: Respiratory Research

    Article Title: LL-37 and citrullinated-LL-37 enhances oxylipins: citrullination attenuates LL-37-mediated COX-2-dependent chemokine response in human bronchial epithelial cells

    doi: 10.1186/s12931-026-03493-w

    Figure Lengend Snippet: Inhibition of COX-2 suppresses LL-37-mediated chemokine production. HBEC-3KT cells were pre-treated with COX-2 inhibitor Rofecoxib (20 nM) for 1 h, followed by stimulation with either LL-37, citLL-37 or sLL-37 (0.50 µM each) for 24 h (n = 5). TC supernatants were examined for the abundance of ( a ) IL-8, ( b ) GROα and ( c ) MIP-3α by ELISA. Chemokine levels shown in pg/mL after background subtraction of levels in unstimulated cells. Each dot represents an independent experiment (n = 5), the bars show IQR with the median line and the whiskers represent the min-max range. Statistical significance was measured using Two-Way ANOVA, and # represents statistical significance compared to unstimulated cells ( ** p < 0.005, *** p < 0.0005, #### or **** p < 0.0001)

    Article Snippet: The abundance of IL-8 (Cat# DY208), GROα (Cat# DY275) and MIP-3α (Cat# DY360) were examined in TC supernatants using ELISA kits obtained from R&D Systems, according to the manufacturer’s instructions.

    Techniques: Inhibition, Enzyme-linked Immunosorbent Assay

    Inhibition of PGE2 receptors (EP1-4) suppresses LL-37-mediated enhancement of chemokines. HBEC-3KT cells were pre-treated with specific inhibitors for PGE2 receptors, EP1 (SC-19220; 20 nM), EP2 (PF-044EP2; 25 nM), EP3 (L-798,106; 20 nM), or EP4 (MF498; 10 nM), 1 h prior to stimulation with either LL-37or sLL-37 (0.50 μM). Tissue culture (TC) supernatants were collected after 24 h and the abundance of ( a ) IL-8, ( b ) GROα and ( c ) MIP-3α were measured by ELISA. Each dot represents an independent experiment (n=4), the bars show IQR with the median line and the whiskers represent the min-max range. Results shown are after subtracting baseline values obtained from unstimulated cells in each independent experiment. Statistical significance was determined using Two-Way ANOVA (** p < 0.001 and **** p < 0.0001)

    Journal: Respiratory Research

    Article Title: LL-37 and citrullinated-LL-37 enhances oxylipins: citrullination attenuates LL-37-mediated COX-2-dependent chemokine response in human bronchial epithelial cells

    doi: 10.1186/s12931-026-03493-w

    Figure Lengend Snippet: Inhibition of PGE2 receptors (EP1-4) suppresses LL-37-mediated enhancement of chemokines. HBEC-3KT cells were pre-treated with specific inhibitors for PGE2 receptors, EP1 (SC-19220; 20 nM), EP2 (PF-044EP2; 25 nM), EP3 (L-798,106; 20 nM), or EP4 (MF498; 10 nM), 1 h prior to stimulation with either LL-37or sLL-37 (0.50 μM). Tissue culture (TC) supernatants were collected after 24 h and the abundance of ( a ) IL-8, ( b ) GROα and ( c ) MIP-3α were measured by ELISA. Each dot represents an independent experiment (n=4), the bars show IQR with the median line and the whiskers represent the min-max range. Results shown are after subtracting baseline values obtained from unstimulated cells in each independent experiment. Statistical significance was determined using Two-Way ANOVA (** p < 0.001 and **** p < 0.0001)

    Article Snippet: The abundance of IL-8 (Cat# DY208), GROα (Cat# DY275) and MIP-3α (Cat# DY360) were examined in TC supernatants using ELISA kits obtained from R&D Systems, according to the manufacturer’s instructions.

    Techniques: Inhibition, Enzyme-linked Immunosorbent Assay

    Proposed mechanism of LL-37-COX-2 axis for chemokine production and neutrophil migration in the lungs. LL-37 engages the P2X 7 receptor in upregulating COX-2 expression which facilitates increase in the abundance of prostaglandin PGE2. Release of PGE2 may act in an autocrine manner through PGE2 receptors (EP1 − 4), resulting in enhanced production of chemokines including IL-8 and GROα, which facilitates neutrophil migration contributing to airway inflammation. However, citrullination of LL-37 dampens this pathway, potentially acting as a regulatory switch that limits the pro-inflammatory functions of LL-37 in the lungs (Figure created in BioRender.com)

    Journal: Respiratory Research

    Article Title: LL-37 and citrullinated-LL-37 enhances oxylipins: citrullination attenuates LL-37-mediated COX-2-dependent chemokine response in human bronchial epithelial cells

    doi: 10.1186/s12931-026-03493-w

    Figure Lengend Snippet: Proposed mechanism of LL-37-COX-2 axis for chemokine production and neutrophil migration in the lungs. LL-37 engages the P2X 7 receptor in upregulating COX-2 expression which facilitates increase in the abundance of prostaglandin PGE2. Release of PGE2 may act in an autocrine manner through PGE2 receptors (EP1 − 4), resulting in enhanced production of chemokines including IL-8 and GROα, which facilitates neutrophil migration contributing to airway inflammation. However, citrullination of LL-37 dampens this pathway, potentially acting as a regulatory switch that limits the pro-inflammatory functions of LL-37 in the lungs (Figure created in BioRender.com)

    Article Snippet: The abundance of IL-8 (Cat# DY208), GROα (Cat# DY275) and MIP-3α (Cat# DY360) were examined in TC supernatants using ELISA kits obtained from R&D Systems, according to the manufacturer’s instructions.

    Techniques: Migration, Expressing

    Increased expression of CXCL1 mRNA levels is associated with the clinical characteristics of patients with RCC. (A) The expression profiles of CXCL1 mRNA in normal tissues compared with ccRCC or pRCC tissues. The different levels of expression of CXCL1 mRNA within (B) different clinical grades and (C) subtypes of ccRCC tissues. Expression levels of CXCL1 mRNA in the (D) GSE53757 and the (E) GSE40435 datasets. The different levels of expression of CXCL1 mRNA within different (F) clinical grades and (G) stages of ccRCC tissues. Analysis of the expression level of CXCL1 within the clinical (H) T-status, (I) N-status and (J) M-status categories in ccRCC tissues. (K-M) A prognostic assessment was performed among the various groups. **P<0.01 vs. normal; # P<0.01 vs. normal, grade 1 and 2; ▲ P<0.01 vs. normal and ccA subtype. CXCL1, CXC motif chemokine ligand 1; RCC, renal cell carcinoma; ccRCC, clear cell RCC; pRCC, papillary RCC; T, tumor; N, lymph node; M, metastasis; OS, overall survival; DSS, disease-specific survival; PFS, progression-free survival.

    Journal: Oncology Letters

    Article Title: Enhanced expression of CXCL1 in renal cell carcinoma facilitates tumor cell malignancy via PI3K/AKT-dependent mechanisms

    doi: 10.3892/ol.2025.15372

    Figure Lengend Snippet: Increased expression of CXCL1 mRNA levels is associated with the clinical characteristics of patients with RCC. (A) The expression profiles of CXCL1 mRNA in normal tissues compared with ccRCC or pRCC tissues. The different levels of expression of CXCL1 mRNA within (B) different clinical grades and (C) subtypes of ccRCC tissues. Expression levels of CXCL1 mRNA in the (D) GSE53757 and the (E) GSE40435 datasets. The different levels of expression of CXCL1 mRNA within different (F) clinical grades and (G) stages of ccRCC tissues. Analysis of the expression level of CXCL1 within the clinical (H) T-status, (I) N-status and (J) M-status categories in ccRCC tissues. (K-M) A prognostic assessment was performed among the various groups. **P<0.01 vs. normal; # P<0.01 vs. normal, grade 1 and 2; ▲ P<0.01 vs. normal and ccA subtype. CXCL1, CXC motif chemokine ligand 1; RCC, renal cell carcinoma; ccRCC, clear cell RCC; pRCC, papillary RCC; T, tumor; N, lymph node; M, metastasis; OS, overall survival; DSS, disease-specific survival; PFS, progression-free survival.

    Article Snippet: Following 24 h culture, the supernatant was isolated via centrifugation at 4°C, 1,000 × g for 5 min, and a Human CXCL1 ELISA kit (cat. no. EK0722; Wuhan Boster Biological Technology, Ltd.) was employed to determine and quantify the level of CXCL1 in the supernatant, following precisely the manufacturer's instructions.

    Techniques: Expressing

    Expression levels of CXCL1 mRNA are correlated with the expression of genes implicated in tumorigenesis, recruitment of immune cells and presence of MSI in renal cell carcinoma. (A) Identification of 10 hub genes exhibiting co-expression with CXCL1. (B) Analysis of the protein-interaction network involving CXCL1. (C) Analysis of the correlation between CXCL1 and the aforementioned 10 hub genes. (D) Analysis of the correlation between CXCL1 expression and immune cell recruitment. The correlation between CXCL1 expression and the (E) number of mutations is presented, as well as (F) MSI scores. (G) The expression levels of CXCL1 in the MSI group compared with the MSS group. *P<0.05; **P<0.01; ***P<0.001; ****P<0.0001. CXCL, CXC motif chemokine ligand; ACKR1, atypical chemokine receptor 1; CCR, C-C chemokine receptor type 2; MSI, microsatellite instability; MSS, microsatellite stable or no apparent MSI; TIMER, tumor immune estimation resource; TCGA, The Cancer Genome Atlas; T, tumor; N, normal.

    Journal: Oncology Letters

    Article Title: Enhanced expression of CXCL1 in renal cell carcinoma facilitates tumor cell malignancy via PI3K/AKT-dependent mechanisms

    doi: 10.3892/ol.2025.15372

    Figure Lengend Snippet: Expression levels of CXCL1 mRNA are correlated with the expression of genes implicated in tumorigenesis, recruitment of immune cells and presence of MSI in renal cell carcinoma. (A) Identification of 10 hub genes exhibiting co-expression with CXCL1. (B) Analysis of the protein-interaction network involving CXCL1. (C) Analysis of the correlation between CXCL1 and the aforementioned 10 hub genes. (D) Analysis of the correlation between CXCL1 expression and immune cell recruitment. The correlation between CXCL1 expression and the (E) number of mutations is presented, as well as (F) MSI scores. (G) The expression levels of CXCL1 in the MSI group compared with the MSS group. *P<0.05; **P<0.01; ***P<0.001; ****P<0.0001. CXCL, CXC motif chemokine ligand; ACKR1, atypical chemokine receptor 1; CCR, C-C chemokine receptor type 2; MSI, microsatellite instability; MSS, microsatellite stable or no apparent MSI; TIMER, tumor immune estimation resource; TCGA, The Cancer Genome Atlas; T, tumor; N, normal.

    Article Snippet: Following 24 h culture, the supernatant was isolated via centrifugation at 4°C, 1,000 × g for 5 min, and a Human CXCL1 ELISA kit (cat. no. EK0722; Wuhan Boster Biological Technology, Ltd.) was employed to determine and quantify the level of CXCL1 in the supernatant, following precisely the manufacturer's instructions.

    Techniques: Expressing

    Protein levels of CXCL1 expression are markedly elevated in the tissues of patients with RCC. Representative images, illustrating strong-intensity staining of CXCL1 in (A) grade I, (B) grade II and (C) grade III RCC tissues. (D) Representative image, illustrating weak-intensity staining of CXCL1 in paracancerous tissues. CXCL1, CXC motif chemokine ligand 1; RCC, renal cell carcinoma.

    Journal: Oncology Letters

    Article Title: Enhanced expression of CXCL1 in renal cell carcinoma facilitates tumor cell malignancy via PI3K/AKT-dependent mechanisms

    doi: 10.3892/ol.2025.15372

    Figure Lengend Snippet: Protein levels of CXCL1 expression are markedly elevated in the tissues of patients with RCC. Representative images, illustrating strong-intensity staining of CXCL1 in (A) grade I, (B) grade II and (C) grade III RCC tissues. (D) Representative image, illustrating weak-intensity staining of CXCL1 in paracancerous tissues. CXCL1, CXC motif chemokine ligand 1; RCC, renal cell carcinoma.

    Article Snippet: Following 24 h culture, the supernatant was isolated via centrifugation at 4°C, 1,000 × g for 5 min, and a Human CXCL1 ELISA kit (cat. no. EK0722; Wuhan Boster Biological Technology, Ltd.) was employed to determine and quantify the level of CXCL1 in the supernatant, following precisely the manufacturer's instructions.

    Techniques: Expressing, Staining

    Exogenous CXCL1 treatment enhances the malignant phenotype of renal cell carcinoma cells. Assessment of cell proliferation using a Cell Counting Kit-8 assay in (A) 786-O and (B) CAKI-2 cells. Representative images from Transwell assays with (C) 786-O and (D) CAKI-2 cells (magnification, ×100). Assessment of cell migration using a Transwell assay in (E) 786-O and (F) CAKI-2 cells. *P<0.05; **P<0.01 vs. 0 ng/ml. CXCL1, CXC motif chemokine ligand 1.

    Journal: Oncology Letters

    Article Title: Enhanced expression of CXCL1 in renal cell carcinoma facilitates tumor cell malignancy via PI3K/AKT-dependent mechanisms

    doi: 10.3892/ol.2025.15372

    Figure Lengend Snippet: Exogenous CXCL1 treatment enhances the malignant phenotype of renal cell carcinoma cells. Assessment of cell proliferation using a Cell Counting Kit-8 assay in (A) 786-O and (B) CAKI-2 cells. Representative images from Transwell assays with (C) 786-O and (D) CAKI-2 cells (magnification, ×100). Assessment of cell migration using a Transwell assay in (E) 786-O and (F) CAKI-2 cells. *P<0.05; **P<0.01 vs. 0 ng/ml. CXCL1, CXC motif chemokine ligand 1.

    Article Snippet: Following 24 h culture, the supernatant was isolated via centrifugation at 4°C, 1,000 × g for 5 min, and a Human CXCL1 ELISA kit (cat. no. EK0722; Wuhan Boster Biological Technology, Ltd.) was employed to determine and quantify the level of CXCL1 in the supernatant, following precisely the manufacturer's instructions.

    Techniques: Cell Counting, Migration, Transwell Assay

    Overexpression of CXCL1 stimulates the malignant phenotype of renal cell carcinoma cells. Evaluation of CXCL3 expression in the supernatant from cell medium using ELISA assay in (A) 786-O and (B) CAKI-2 cells. Assessment of cell proliferation using a Cell Counting Kit-8 assay with (C) 786-O and (D) CAKI-2 cells. Representative images from Transwell assay experiments with (E) 786-O and (F) CAKI-2 cells (magnification, ×100). Assessment of cell migration using Transwell assay with (G) 786-O and (H) CAKI-2 cells. **P<0.01 vs. control. CXCL1, CXC motif chemokine ligand 1.

    Journal: Oncology Letters

    Article Title: Enhanced expression of CXCL1 in renal cell carcinoma facilitates tumor cell malignancy via PI3K/AKT-dependent mechanisms

    doi: 10.3892/ol.2025.15372

    Figure Lengend Snippet: Overexpression of CXCL1 stimulates the malignant phenotype of renal cell carcinoma cells. Evaluation of CXCL3 expression in the supernatant from cell medium using ELISA assay in (A) 786-O and (B) CAKI-2 cells. Assessment of cell proliferation using a Cell Counting Kit-8 assay with (C) 786-O and (D) CAKI-2 cells. Representative images from Transwell assay experiments with (E) 786-O and (F) CAKI-2 cells (magnification, ×100). Assessment of cell migration using Transwell assay with (G) 786-O and (H) CAKI-2 cells. **P<0.01 vs. control. CXCL1, CXC motif chemokine ligand 1.

    Article Snippet: Following 24 h culture, the supernatant was isolated via centrifugation at 4°C, 1,000 × g for 5 min, and a Human CXCL1 ELISA kit (cat. no. EK0722; Wuhan Boster Biological Technology, Ltd.) was employed to determine and quantify the level of CXCL1 in the supernatant, following precisely the manufacturer's instructions.

    Techniques: Over Expression, Expressing, Enzyme-linked Immunosorbent Assay, Cell Counting, Transwell Assay, Migration, Control

    Low expression of CXCL1 suppresses the malignant phenotype of renal cell carcinoma cells. Evaluation of CXCL3 expression in the supernatant from cell medium using ELISA assay with (A) 786-O and (B) CAKI-2 cells. Assessment of cell proliferation using a Cell Counting Kit-8 assay with (C) 786-O and (D) CAKI-2 cells. Representative images from Transwell assay experiments (magnification, ×100) with (E) 786-O and (F) CAKI-2 cells. Assessment of cell migration using Transwell assay with (G) 786-O and (H) CAKI-2 cells. **P<0.1 01 vs. control. CXCL1, CXC motif chemokine ligand 1; siRNA, small interfering RNA.

    Journal: Oncology Letters

    Article Title: Enhanced expression of CXCL1 in renal cell carcinoma facilitates tumor cell malignancy via PI3K/AKT-dependent mechanisms

    doi: 10.3892/ol.2025.15372

    Figure Lengend Snippet: Low expression of CXCL1 suppresses the malignant phenotype of renal cell carcinoma cells. Evaluation of CXCL3 expression in the supernatant from cell medium using ELISA assay with (A) 786-O and (B) CAKI-2 cells. Assessment of cell proliferation using a Cell Counting Kit-8 assay with (C) 786-O and (D) CAKI-2 cells. Representative images from Transwell assay experiments (magnification, ×100) with (E) 786-O and (F) CAKI-2 cells. Assessment of cell migration using Transwell assay with (G) 786-O and (H) CAKI-2 cells. **P<0.1 01 vs. control. CXCL1, CXC motif chemokine ligand 1; siRNA, small interfering RNA.

    Article Snippet: Following 24 h culture, the supernatant was isolated via centrifugation at 4°C, 1,000 × g for 5 min, and a Human CXCL1 ELISA kit (cat. no. EK0722; Wuhan Boster Biological Technology, Ltd.) was employed to determine and quantify the level of CXCL1 in the supernatant, following precisely the manufacturer's instructions.

    Techniques: Expressing, Enzyme-linked Immunosorbent Assay, Cell Counting, Transwell Assay, Migration, Control, Small Interfering RNA

    Overexpression of CXCL1 modulates the expression of PI3K/AKT pathway-associated proteins in renal cell carcinoma cells. Representative images from western blotting assays in (A) 786-O and (B) CAKI-2 cells. Semi-quantification of the protein expression levels of Bax, Bcl-2, PI3K and AKT in (C) 786-O and (D) CAKI-2 cells. **P<0.01 vs. control. CXCL1, CXC motif chemokine ligand 1; Bax, Bcl-2-associated X protein; Bcl-2, B-cell lymphoma-2; PI3K, phosphoinositide 3-kinase.

    Journal: Oncology Letters

    Article Title: Enhanced expression of CXCL1 in renal cell carcinoma facilitates tumor cell malignancy via PI3K/AKT-dependent mechanisms

    doi: 10.3892/ol.2025.15372

    Figure Lengend Snippet: Overexpression of CXCL1 modulates the expression of PI3K/AKT pathway-associated proteins in renal cell carcinoma cells. Representative images from western blotting assays in (A) 786-O and (B) CAKI-2 cells. Semi-quantification of the protein expression levels of Bax, Bcl-2, PI3K and AKT in (C) 786-O and (D) CAKI-2 cells. **P<0.01 vs. control. CXCL1, CXC motif chemokine ligand 1; Bax, Bcl-2-associated X protein; Bcl-2, B-cell lymphoma-2; PI3K, phosphoinositide 3-kinase.

    Article Snippet: Following 24 h culture, the supernatant was isolated via centrifugation at 4°C, 1,000 × g for 5 min, and a Human CXCL1 ELISA kit (cat. no. EK0722; Wuhan Boster Biological Technology, Ltd.) was employed to determine and quantify the level of CXCL1 in the supernatant, following precisely the manufacturer's instructions.

    Techniques: Over Expression, Expressing, Western Blot, Control

    Blocking AKT reverses the promoting effect of overexpression of CXCL1 on the malignant behaviors of renal cell carcinoma cells. Assessment of cell proliferation using a Cell Counting Kit-8 assay in (A) 786-O and (B) CAKI-2 cells. (Representative images from Transwell assay experiments (magnification, ×100) with (C) 786-O and (D) CAKI-2 cells. Assessment of cell migration using Transwell assay with (E) 786-O and (F) CAKI-2 cells. (magnification, ×100). **P<0.01 compared with overexpression. CXCL1, CXC motif chemokine ligand 1.

    Journal: Oncology Letters

    Article Title: Enhanced expression of CXCL1 in renal cell carcinoma facilitates tumor cell malignancy via PI3K/AKT-dependent mechanisms

    doi: 10.3892/ol.2025.15372

    Figure Lengend Snippet: Blocking AKT reverses the promoting effect of overexpression of CXCL1 on the malignant behaviors of renal cell carcinoma cells. Assessment of cell proliferation using a Cell Counting Kit-8 assay in (A) 786-O and (B) CAKI-2 cells. (Representative images from Transwell assay experiments (magnification, ×100) with (C) 786-O and (D) CAKI-2 cells. Assessment of cell migration using Transwell assay with (E) 786-O and (F) CAKI-2 cells. (magnification, ×100). **P<0.01 compared with overexpression. CXCL1, CXC motif chemokine ligand 1.

    Article Snippet: Following 24 h culture, the supernatant was isolated via centrifugation at 4°C, 1,000 × g for 5 min, and a Human CXCL1 ELISA kit (cat. no. EK0722; Wuhan Boster Biological Technology, Ltd.) was employed to determine and quantify the level of CXCL1 in the supernatant, following precisely the manufacturer's instructions.

    Techniques: Blocking Assay, Over Expression, Cell Counting, Transwell Assay, Migration