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cc motif chemokine ligand 8 (R&D Systems)

Name: cc motif chemokine ligand 8
Brand: R&D Systems
Rating: 93 (10 reviews)

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R&D Systems cc motif chemokine ligand 8
a) Pan CD8 T cells migrated towards CXCL2 (at all dilutions for donor 1, and at 1 ng/ml and 10 ng/ml for donor 2), b) pan monocytes did not migrate towards RARRES2, c) pan monocytes migrated towards <t>CCL8</t> (at 0.1 ng/ml, 1 ng/ml and 100 ng/ml for donor 1, and at 0.1 ng/ml and 100 ng/ml for donor 2).* p < 0.05. ** p < 0.01, *** p < 0.0001 compared to the medium control condition per donor.

a) Pan CD8 T cells migrated towards CXCL2 (at all dilutions for donor 1, and at 1 ng/ml and 10 ng/ml for donor 2), b) pan monocytes did not migrate towards RARRES2, c) pan monocytes migrated towards <t>CCL8</t> (at 0.1 ng/ml, 1 ng/ml and 100 ng/ml for donor 1, and at 0.1 ng/ml and 100 ng/ml for donor 2).* p < 0.05. ** p < 0.01, *** p < 0.0001 compared to the medium control condition per donor.

Cc Motif Chemokine Ligand 8, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/cc motif chemokine ligand 8/product/R&D Systems
Average 93 stars, based on 10 article reviews

cc motif chemokine ligand 8 - by Bioz Stars, 2026-03

93/100 stars

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1) Product Images from "Immune disease dialogue of chemokine-based cell communications as revealed by single-cell RNA sequencing meta-analysis"

Article Title: Immune disease dialogue of chemokine-based cell communications as revealed by single-cell RNA sequencing meta-analysis

Journal: bioRxiv

doi: 10.1101/2024.07.17.603936

Figure Legend Snippet: a) Pan CD8 T cells migrated towards CXCL2 (at all dilutions for donor 1, and at 1 ng/ml and 10 ng/ml for donor 2), b) pan monocytes did not migrate towards RARRES2, c) pan monocytes migrated towards CCL8 (at 0.1 ng/ml, 1 ng/ml and 100 ng/ml for donor 1, and at 0.1 ng/ml and 100 ng/ml for donor 2).* p < 0.05. ** p < 0.01, *** p < 0.0001 compared to the medium control condition per donor.

Techniques Used: Control

Image Search Results

A) Top four highly secreted cytokines in CM from astrocytes overexpressing miR-425 as measured by cytokine arrays. B) Cytokine stimulation increases GFAP expression in human astrocytes as indicated by GFAP IF. Representative 20x images. Scale bar indicates 100 µm. C) CCL8, SCF, and MIF stimulation promotes SKBR3 mammospheres. Scale bar indicates 100 µm. D) CCL8 and SCF promote mammosphere formation of CN34 cells. Scale bar indicates 100 µm. E) CCL8 and KITLG are upregulated in astrocytes overexpressing miR-425 as measured by RT-qPCR. F) Human astrocytes stimulated by CM from SKBR3 cells overexpressing miR-425 secrete significantly higher levels of CCL8 compared to astrocytes stimulated with CM from control SKBR3 cells. Secreted CCL8 expression measured by ELISA. G) Astrocytes stimulated by CM from CN34 overexpressing miR-425 secrete significantly increased levels of CCL8 compared to astrocytes stimulated with CM from control CN34 cells. Secreted CCL8 expression measured by ELISA. H-I) Astrocytes stimulated by CM from SKBR3 or CN34 cells overexpressing miR-425 secrete high levels of SCF. Secreted SCF expression measured by ELISA. Fold change was calculated in Panels E. Student’s t -test was used in Panels B-I. N = 3 experimental replicates unless otherwise indicated.

Journal: bioRxiv

Article Title: Extracellular vesicle-derived miR-425-5p (miR-425) activates astrocytes in the brain to promote breast cancer brain metastasis via the novel miR-425-ZNF24-CCL8 signaling axis

doi: 10.1101/2025.06.05.658130

Figure Lengend Snippet: A) Top four highly secreted cytokines in CM from astrocytes overexpressing miR-425 as measured by cytokine arrays. B) Cytokine stimulation increases GFAP expression in human astrocytes as indicated by GFAP IF. Representative 20x images. Scale bar indicates 100 µm. C) CCL8, SCF, and MIF stimulation promotes SKBR3 mammospheres. Scale bar indicates 100 µm. D) CCL8 and SCF promote mammosphere formation of CN34 cells. Scale bar indicates 100 µm. E) CCL8 and KITLG are upregulated in astrocytes overexpressing miR-425 as measured by RT-qPCR. F) Human astrocytes stimulated by CM from SKBR3 cells overexpressing miR-425 secrete significantly higher levels of CCL8 compared to astrocytes stimulated with CM from control SKBR3 cells. Secreted CCL8 expression measured by ELISA. G) Astrocytes stimulated by CM from CN34 overexpressing miR-425 secrete significantly increased levels of CCL8 compared to astrocytes stimulated with CM from control CN34 cells. Secreted CCL8 expression measured by ELISA. H-I) Astrocytes stimulated by CM from SKBR3 or CN34 cells overexpressing miR-425 secrete high levels of SCF. Secreted SCF expression measured by ELISA. Fold change was calculated in Panels E. Student’s t -test was used in Panels B-I. N = 3 experimental replicates unless otherwise indicated.

Article Snippet: Astrocytes were transfected with control or miR-425 mimic, control vector or ZNF24 3’UTR (GeneCopoeia; Cs-HmiT119980-MT05-01), control vector or ZNF24 overexpression (VB221017-1240ueu), and control promoter or CCL8 promoter (GeneCopoeia; HPRM46246-PG02) constructs using X-tremeGENE HP DNA Transfection Reagent (Millipore Sigma; 6366244001).

Techniques: Expressing, Quantitative RT-PCR, Control, Enzyme-linked Immunosorbent Assay

A) Predicted miR-425 binding sites within the CREB1, BCOR, and ZNF24 3’-UTRs from TargetScan. B) ZNF24 mRNA expression is significantly decreased in astrocytes overexpressing miR-425. CREB1 and BCOR mRNA expression is unchanged as measured by RT-qPCR. C) ZNF24 protein expression is decreased in astrocytes transfected with miR-425 mimic as indicated by western blot analysis. D) miR-425 suppresses ZNF24 3’-UTR activity as measured by dual luciferase reporter assay. E) Ectopic expression of ZNF24 significantly decreases CCL8 and VEGFA mRNA expression, while KITLG is unchanged. mRNA expression measured by RT-qPCR. F) Ectopic expression of ZNF24 suppresses CCL8 protein expression, but not SCF as indicated by western blot analysis. G) ZNF24 knockdown significantly increases CCL8 and VEGFA mRNA expression, but not KITLG. mRNA expression as indicated by RT-qPCR. H) ZNF24 knockdown increases CCL8 and SCF protein expression as measured by western blot analysis. Fold change was calculated in Panels B, D, E, and G. Student’s t- test was used in Panels B, D, E, and G. N = 3 experimental replicates unless otherwise indicated.

Journal: bioRxiv

Article Title: Extracellular vesicle-derived miR-425-5p (miR-425) activates astrocytes in the brain to promote breast cancer brain metastasis via the novel miR-425-ZNF24-CCL8 signaling axis

doi: 10.1101/2025.06.05.658130

Figure Lengend Snippet: A) Predicted miR-425 binding sites within the CREB1, BCOR, and ZNF24 3’-UTRs from TargetScan. B) ZNF24 mRNA expression is significantly decreased in astrocytes overexpressing miR-425. CREB1 and BCOR mRNA expression is unchanged as measured by RT-qPCR. C) ZNF24 protein expression is decreased in astrocytes transfected with miR-425 mimic as indicated by western blot analysis. D) miR-425 suppresses ZNF24 3’-UTR activity as measured by dual luciferase reporter assay. E) Ectopic expression of ZNF24 significantly decreases CCL8 and VEGFA mRNA expression, while KITLG is unchanged. mRNA expression measured by RT-qPCR. F) Ectopic expression of ZNF24 suppresses CCL8 protein expression, but not SCF as indicated by western blot analysis. G) ZNF24 knockdown significantly increases CCL8 and VEGFA mRNA expression, but not KITLG. mRNA expression as indicated by RT-qPCR. H) ZNF24 knockdown increases CCL8 and SCF protein expression as measured by western blot analysis. Fold change was calculated in Panels B, D, E, and G. Student’s t- test was used in Panels B, D, E, and G. N = 3 experimental replicates unless otherwise indicated.

Techniques: Binding Assay, Expressing, Quantitative RT-PCR, Transfection, Western Blot, Activity Assay, Luciferase, Reporter Assay, Knockdown

A) Human astrocytes activated by a cocktail of IL-1α, TNFα, and C1q. Representative 20x images. Scale bar indicates 100 µm. B) Validation of GFAP mRNA expression in activated astrocytes as indicated by RT-qPCR. C) Activated astrocytes transfected with ZNF24 plasmid have significantly reduced GFAP expression as indicated by GFAP IF. Representative 20x images. Scale bar indicates 100 µm. D) Validation of GFAP reduction and ZNF24 overexpression with ectopic expression of ZNF24. mRNA expression measured by RT-qPCR. E) ZNF24 binding to the CCL8 promoter in two regions (−69 and -205 bases upstream of the TSS) measured by ChIP-qPCR. F) Ectopic expression of ZNF24 suppresses CCL8 promoter activity as indicated by dual luciferase reporter assays. G-H) ZNF24 and CCL8 mRNA expression remains unchanged in breast cancer cells transfected with control or miR-425 mimic. mRNA expression measured by RT-qPCR. Fold change was calculated in Panels B, D-H. Student’s t -test was used in Panels A-H. N = 3 experimental replicates unless otherwise indicated.

Journal: bioRxiv

Article Title: Extracellular vesicle-derived miR-425-5p (miR-425) activates astrocytes in the brain to promote breast cancer brain metastasis via the novel miR-425-ZNF24-CCL8 signaling axis

doi: 10.1101/2025.06.05.658130

Figure Lengend Snippet: A) Human astrocytes activated by a cocktail of IL-1α, TNFα, and C1q. Representative 20x images. Scale bar indicates 100 µm. B) Validation of GFAP mRNA expression in activated astrocytes as indicated by RT-qPCR. C) Activated astrocytes transfected with ZNF24 plasmid have significantly reduced GFAP expression as indicated by GFAP IF. Representative 20x images. Scale bar indicates 100 µm. D) Validation of GFAP reduction and ZNF24 overexpression with ectopic expression of ZNF24. mRNA expression measured by RT-qPCR. E) ZNF24 binding to the CCL8 promoter in two regions (−69 and -205 bases upstream of the TSS) measured by ChIP-qPCR. F) Ectopic expression of ZNF24 suppresses CCL8 promoter activity as indicated by dual luciferase reporter assays. G-H) ZNF24 and CCL8 mRNA expression remains unchanged in breast cancer cells transfected with control or miR-425 mimic. mRNA expression measured by RT-qPCR. Fold change was calculated in Panels B, D-H. Student’s t -test was used in Panels A-H. N = 3 experimental replicates unless otherwise indicated.

Techniques: Biomarker Discovery, Expressing, Quantitative RT-PCR, Transfection, Plasmid Preparation, Over Expression, Binding Assay, ChIP-qPCR, Activity Assay, Luciferase, Control

A) Increased EV-miR-425 expression in mouse serum from the SKBR3-Luc-miR-425 group compared to the control group. miR-425 expression measured by RT-qPCR (N = 5 per group). B) SKBR3-Luc-miR-425 group mouse serum has significantly higher levels of mouse CCL8 as measured by ELISA (N = 7 per group). C) No significant difference in mouse SCF levels in SKBR3-Luc-miR-425 or control mice serum as measured by ELISA (N = 5 per group). D-E) GFAP H-score and intratumoral astrocytes are significantly higher in brain metastases from the SKBR3-Luc-miR-425 mouse group than the control in mouse brain sections as measured by IHC (N = 5 per group). F) Brain metastases from the SKBR3-Luc-miR-425 group have significantly increased Ki-67 positive cells as measured by IHC (N = 5 per group). G) Tumor-adjacent and infiltrative astrocytes in brain metastases from the SKBR3-Luc-miR-425 group have decreased ZNF24 staining measured by IHC (N = 5 per group). H) Representative IHC images at 20x magnification. Scale bar indicates 100 µm. I) Co-staining IF of ZNF24 and GFAP in mouse brain sections containing brain metastases. Representative images at 20x magnification. Scale bar indicates 100 µm. J) Schematic of described mechanism by which breast cancer-derived EV-miR-425 activates astrocytes by suppressing ZNF24, increasing CCL8, and thereby promoting BCBM. Fold change was calculated in Panel A. Student’s t -test used in Panels A-G, and I.

Journal: bioRxiv

Article Title: Extracellular vesicle-derived miR-425-5p (miR-425) activates astrocytes in the brain to promote breast cancer brain metastasis via the novel miR-425-ZNF24-CCL8 signaling axis

doi: 10.1101/2025.06.05.658130

Figure Lengend Snippet: A) Increased EV-miR-425 expression in mouse serum from the SKBR3-Luc-miR-425 group compared to the control group. miR-425 expression measured by RT-qPCR (N = 5 per group). B) SKBR3-Luc-miR-425 group mouse serum has significantly higher levels of mouse CCL8 as measured by ELISA (N = 7 per group). C) No significant difference in mouse SCF levels in SKBR3-Luc-miR-425 or control mice serum as measured by ELISA (N = 5 per group). D-E) GFAP H-score and intratumoral astrocytes are significantly higher in brain metastases from the SKBR3-Luc-miR-425 mouse group than the control in mouse brain sections as measured by IHC (N = 5 per group). F) Brain metastases from the SKBR3-Luc-miR-425 group have significantly increased Ki-67 positive cells as measured by IHC (N = 5 per group). G) Tumor-adjacent and infiltrative astrocytes in brain metastases from the SKBR3-Luc-miR-425 group have decreased ZNF24 staining measured by IHC (N = 5 per group). H) Representative IHC images at 20x magnification. Scale bar indicates 100 µm. I) Co-staining IF of ZNF24 and GFAP in mouse brain sections containing brain metastases. Representative images at 20x magnification. Scale bar indicates 100 µm. J) Schematic of described mechanism by which breast cancer-derived EV-miR-425 activates astrocytes by suppressing ZNF24, increasing CCL8, and thereby promoting BCBM. Fold change was calculated in Panel A. Student’s t -test used in Panels A-G, and I.

Techniques: Expressing, Control, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Staining, Derivative Assay

Journal: bioRxiv

Article Title: Immune disease dialogue of chemokine-based cell communications as revealed by single-cell RNA sequencing meta-analysis

doi: 10.1101/2024.07.17.603936

Figure Lengend Snippet: a) Pan CD8 T cells migrated towards CXCL2 (at all dilutions for donor 1, and at 1 ng/ml and 10 ng/ml for donor 2), b) pan monocytes did not migrate towards RARRES2, c) pan monocytes migrated towards CCL8 (at 0.1 ng/ml, 1 ng/ml and 100 ng/ml for donor 1, and at 0.1 ng/ml and 100 ng/ml for donor 2).* p < 0.05. ** p < 0.01, *** p < 0.0001 compared to the medium control condition per donor.

Article Snippet: For the monocyte experiments, two positive controls were used; 5% (v/v) cobra venom activated human complement serum (CAS; Complement Technology Inc, cat. NC1769554), as well as CC motif chemokine ligand 8 (CCL8; R&D Systems, cat. 281-CP-010).

Techniques: Control

Journal: Cancers

Article Title: Lactate-Induced CCL8 in Tumor-Associated Macrophages Accelerates the Progression of Colorectal Cancer through the CCL8/CCR5/mTORC1 Axis

doi: 10.3390/cancers15245795

Figure Lengend Snippet: Primer sequences.

Article Snippet: Recombinant human CCL8 (rCCL8) protein, macrophage colony-stimulating factor (MCSF), and Maraviroc (selective antagonist of CCR5) were purchased from MCE.

Techniques: Sequencing

Journal: Cancers

Article Title: Lactate-Induced CCL8 in Tumor-Associated Macrophages Accelerates the Progression of Colorectal Cancer through the CCL8/CCR5/mTORC1 Axis

doi: 10.3390/cancers15245795

Figure Lengend Snippet: Antibody list.

Article Snippet: Recombinant human CCL8 (rCCL8) protein, macrophage colony-stimulating factor (MCSF), and Maraviroc (selective antagonist of CCR5) were purchased from MCE.

Techniques:

CCL8 was induced by lactate in macrophages. ( A , B ) KEGG pathway and volcano map and volcano map analysis of differential genes on lactate-treated macrophages for 24 h. ( C ) qRT-PCR in macrophages stimulated with CM3 or LA for 24 h. ( D ) ELISA detection of CCL8 in the serum of healthy and CRC donors. ( E , F ) Representative images and quantitative analysis of immunohistochemistry for CCL8 and CD68 in CRC tissues and adjacent nontumor tissues. All t -tests were two-tailed. Mean ± SEM. ** p < 0.01; *** p < 0.001. Scale bar: 100 μm.

Journal: Cancers

Article Title: Lactate-Induced CCL8 in Tumor-Associated Macrophages Accelerates the Progression of Colorectal Cancer through the CCL8/CCR5/mTORC1 Axis

doi: 10.3390/cancers15245795

Figure Lengend Snippet: CCL8 was induced by lactate in macrophages. ( A , B ) KEGG pathway and volcano map and volcano map analysis of differential genes on lactate-treated macrophages for 24 h. ( C ) qRT-PCR in macrophages stimulated with CM3 or LA for 24 h. ( D ) ELISA detection of CCL8 in the serum of healthy and CRC donors. ( E , F ) Representative images and quantitative analysis of immunohistochemistry for CCL8 and CD68 in CRC tissues and adjacent nontumor tissues. All t -tests were two-tailed. Mean ± SEM. ** p < 0.01; *** p < 0.001. Scale bar: 100 μm.

Article Snippet: Recombinant human CCL8 (rCCL8) protein, macrophage colony-stimulating factor (MCSF), and Maraviroc (selective antagonist of CCR5) were purchased from MCE.

Techniques: Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Immunohistochemistry, Two Tailed Test

RNA sequencing analysis of M2-macrophage-related chemokines in macrophages treated with lactate for 24 h.

Journal: Cancers

Article Title: Lactate-Induced CCL8 in Tumor-Associated Macrophages Accelerates the Progression of Colorectal Cancer through the CCL8/CCR5/mTORC1 Axis

doi: 10.3390/cancers15245795

Figure Lengend Snippet: RNA sequencing analysis of M2-macrophage-related chemokines in macrophages treated with lactate for 24 h.

Article Snippet: Recombinant human CCL8 (rCCL8) protein, macrophage colony-stimulating factor (MCSF), and Maraviroc (selective antagonist of CCR5) were purchased from MCE.

Techniques: RNA Sequencing

( A ) Western blot analysis of CCR5 in CRC tissue and adjacent nontumor tissue. ( B , C ) Representative images and quantitative analysis of the colony assay in HCT-116 and RKO cells treated with PBS, CCL8, or CCL8+Maraviroc for 15 days. ( D , E ) Representative images of the immunohistochemistry for skeleton proteins (F-actin and p-SMAD2) in RKO and HCT-116 cells treated with PBS, CCL8, or CCL8+Maraviroc for 24 h. ( F ) Western blot analysis of EMT-related proteins (PCNA, vimentin, N-cadherin) in RKO cells stimulated with CCL8, Maraviroc, or both for 24 h. ( G – K ) Representative images and quantitative analysis of subcutaneous and lung metastasis models of Balb/c-nude tumor-bearing mice, treated with PBS, CCL8, or CCL8 + Maraviroc. All t -tests were two-tailed. Mean ± SEM. * p < 0.05, ** p < 0.01; *** p < 0.001; ns, no significance. Original western blots are presented in . Scale bar: 100 μm.

Journal: Cancers

Article Title: Lactate-Induced CCL8 in Tumor-Associated Macrophages Accelerates the Progression of Colorectal Cancer through the CCL8/CCR5/mTORC1 Axis

doi: 10.3390/cancers15245795

Figure Lengend Snippet: ( A ) Western blot analysis of CCR5 in CRC tissue and adjacent nontumor tissue. ( B , C ) Representative images and quantitative analysis of the colony assay in HCT-116 and RKO cells treated with PBS, CCL8, or CCL8+Maraviroc for 15 days. ( D , E ) Representative images of the immunohistochemistry for skeleton proteins (F-actin and p-SMAD2) in RKO and HCT-116 cells treated with PBS, CCL8, or CCL8+Maraviroc for 24 h. ( F ) Western blot analysis of EMT-related proteins (PCNA, vimentin, N-cadherin) in RKO cells stimulated with CCL8, Maraviroc, or both for 24 h. ( G – K ) Representative images and quantitative analysis of subcutaneous and lung metastasis models of Balb/c-nude tumor-bearing mice, treated with PBS, CCL8, or CCL8 + Maraviroc. All t -tests were two-tailed. Mean ± SEM. * p < 0.05, ** p < 0.01; *** p < 0.001; ns, no significance. Original western blots are presented in . Scale bar: 100 μm.

Article Snippet: Recombinant human CCL8 (rCCL8) protein, macrophage colony-stimulating factor (MCSF), and Maraviroc (selective antagonist of CCR5) were purchased from MCE.

Techniques: Western Blot, Colony Assay, Immunohistochemistry, Two Tailed Test

( A – C ) The alterations of the mTOR/4EBP1/70S6K signaling pathway in RKO cells, after treatment with CCL8, Maraviroc, or a series of combinations of CCL8 and Maraviroc for 24 h. ( D ) The alterations in the mTOR/4EBP1/70S6K signaling pathway in RKO cells before and after CCR5 knockdown, treated with or without CCL8 for 24 h. Original western blots are presented in .

Journal: Cancers

Article Title: Lactate-Induced CCL8 in Tumor-Associated Macrophages Accelerates the Progression of Colorectal Cancer through the CCL8/CCR5/mTORC1 Axis

doi: 10.3390/cancers15245795

Figure Lengend Snippet: ( A – C ) The alterations of the mTOR/4EBP1/70S6K signaling pathway in RKO cells, after treatment with CCL8, Maraviroc, or a series of combinations of CCL8 and Maraviroc for 24 h. ( D ) The alterations in the mTOR/4EBP1/70S6K signaling pathway in RKO cells before and after CCR5 knockdown, treated with or without CCL8 for 24 h. Original western blots are presented in .

Article Snippet: Recombinant human CCL8 (rCCL8) protein, macrophage colony-stimulating factor (MCSF), and Maraviroc (selective antagonist of CCR5) were purchased from MCE.

Techniques: Knockdown, Western Blot

Schematic model showing the tumor-progression-promoting interaction between CRC cells and TAMs. Tumor-associated macrophages (TAMs) are more likely to adopt an M2-type polarization in response to the high lactate level in the tumor microenvironment. This leads to an increase in the secretion of CCL8 by polarized TAMs, which binds to the CCR5 receptor on tumor cells and promotes their proliferation and metastasis via the mTOR/70S6K/4EBP1 signaling pathway.

Journal: Cancers

Article Title: Lactate-Induced CCL8 in Tumor-Associated Macrophages Accelerates the Progression of Colorectal Cancer through the CCL8/CCR5/mTORC1 Axis

doi: 10.3390/cancers15245795

Figure Lengend Snippet: Schematic model showing the tumor-progression-promoting interaction between CRC cells and TAMs. Tumor-associated macrophages (TAMs) are more likely to adopt an M2-type polarization in response to the high lactate level in the tumor microenvironment. This leads to an increase in the secretion of CCL8 by polarized TAMs, which binds to the CCR5 receptor on tumor cells and promotes their proliferation and metastasis via the mTOR/70S6K/4EBP1 signaling pathway.

Article Snippet: Recombinant human CCL8 (rCCL8) protein, macrophage colony-stimulating factor (MCSF), and Maraviroc (selective antagonist of CCR5) were purchased from MCE.

Techniques:

Bioinformatics analysis of the correlation between CCL8 and FMD. A Differential gene expression (GEO database, dataset GSE50712, Control vs. EVE-treated breast tumor bearing mice) is determined using GEO2R; the log-fold-change is used to rank the genes. B – D The expression of CCL8, TGFB1, and HGF in invasive breast cancer samples from the TCGA database. E KEGG enrichment analysis for data from the GEO database (dataset GSE37956, control vs. bevacizumab treated glioblastoma xenograft tumor). F The expression of CCL8, TGFB1, PKG1, LDHA, and HIF1A in GEO database (dataset GSE37956, control vs. bevacizumab treated glioblastoma xenograft tumor). G , H Correlation between CCL8, TGFBI and immune cell infiltration in invasive breast cancer samples from the TCGA database. I GSVA analysis of correlation between CCL8, hypoxia (Gene set from GESA M34030), glycolysis (Gene set from GESA M5113), glucose starvation (Gene set from GESA M15497), mTOR (Gene set from GESA M2672), macrophage (Gene set from GESA M39708), M2 macrophage (Gene set from GESA M8527), M1 macrophage (Gene set from GESA M6586) in invasive breast cancer samples from the TCGA database

Journal: Journal of Translational Medicine

Article Title: Fasting mimicking diet inhibits tumor-associated macrophage survival and pro-tumor function in hypoxia: implications for combination therapy with anti-angiogenic agent

doi: 10.1186/s12967-023-04577-7

Figure Lengend Snippet: Bioinformatics analysis of the correlation between CCL8 and FMD. A Differential gene expression (GEO database, dataset GSE50712, Control vs. EVE-treated breast tumor bearing mice) is determined using GEO2R; the log-fold-change is used to rank the genes. B – D The expression of CCL8, TGFB1, and HGF in invasive breast cancer samples from the TCGA database. E KEGG enrichment analysis for data from the GEO database (dataset GSE37956, control vs. bevacizumab treated glioblastoma xenograft tumor). F The expression of CCL8, TGFB1, PKG1, LDHA, and HIF1A in GEO database (dataset GSE37956, control vs. bevacizumab treated glioblastoma xenograft tumor). G , H Correlation between CCL8, TGFBI and immune cell infiltration in invasive breast cancer samples from the TCGA database. I GSVA analysis of correlation between CCL8, hypoxia (Gene set from GESA M34030), glycolysis (Gene set from GESA M5113), glucose starvation (Gene set from GESA M15497), mTOR (Gene set from GESA M2672), macrophage (Gene set from GESA M39708), M2 macrophage (Gene set from GESA M8527), M1 macrophage (Gene set from GESA M6586) in invasive breast cancer samples from the TCGA database

Article Snippet: Lactate acid assay kit (NJJCBIO, Wuhan, China); glucose assay kit (NJJCBIO, Wuhan, China); cell counting kit-8 assay (Meilun, Dalian, China); human and mouse CCL8 mini ABTS ELISA development kit (PeproTech, Hamburg, Germany).

Techniques: Expressing

FMD inhibits the secretion of CCL8 by TAMs. A Serum CCL8 level in mice is detected by ELISA (* P < 0.05, vs. respective control group, # P < 0.05, vs. respective TAM group). B CCL8 secretion from TAMs treated for 24 h with GD or EVE (100 nM) or 2-DG (10 mM), or 2ME2 (10 µM) is determined by ELISA (* P < 0.05, vs. respective TAM group). C CCL8 mRNA levels in TAMs are determined by RT-PCR (* P < 0.05, vs. respective TAM group). D Migration of MDA-MB-231 cells, after co-incubation with TAMs and low (L) or high doses (H) of CCL8 antibody, is determined in a transwell assay (magnification, ×40)

Journal: Journal of Translational Medicine

Article Title: Fasting mimicking diet inhibits tumor-associated macrophage survival and pro-tumor function in hypoxia: implications for combination therapy with anti-angiogenic agent

doi: 10.1186/s12967-023-04577-7

Figure Lengend Snippet: FMD inhibits the secretion of CCL8 by TAMs. A Serum CCL8 level in mice is detected by ELISA (* P < 0.05, vs. respective control group, # P < 0.05, vs. respective TAM group). B CCL8 secretion from TAMs treated for 24 h with GD or EVE (100 nM) or 2-DG (10 mM), or 2ME2 (10 µM) is determined by ELISA (* P < 0.05, vs. respective TAM group). C CCL8 mRNA levels in TAMs are determined by RT-PCR (* P < 0.05, vs. respective TAM group). D Migration of MDA-MB-231 cells, after co-incubation with TAMs and low (L) or high doses (H) of CCL8 antibody, is determined in a transwell assay (magnification, ×40)

Techniques: Enzyme-linked Immunosorbent Assay, Reverse Transcription Polymerase Chain Reaction, Migration, Incubation, Transwell Assay

M1 and M2 macrophages were co-cultured with BLM melanoma cells for transcriptomic (24 h) and secretomic (72 h) analyses. (A) Gene set enrichment analyses (GSEA) comparing 24 hours exposed vs un-exposed isolated cells, as indicated (n=3 donors). Normalized Enrichment Score (NES) values from the main upregulated hallmark_pathwaysfor all groups,are shown. GOMF and KEGG gene sets were additionally studied for cytokine/ chemokine inflammatory pathways. False Discovery Rates are represented (FDR q value <0.01). (B) Representative scheme highlighting the coincident most upregulated secreted chemokines (fold >4 to both unex-posed macrophages and melanoma cells). (C) Secretomic analysis (38 chemokines) of 72 hours co-cultured supernatants comparing M1+ BLM or M2+BLM with unexposed macrophages (x-axis) or BLM (y-axis) cells. Fold logarithmic average changes are shown (n=4 donors). (D) CCL8 and CCL15 secretion assessed at 72 h macrophages ±BLM conditioned media. Mean ±standard deviation (SD) values are shown (n= 5 do-nors). (E) CCL8 and CCL15 mRNA expression levels in mutually conditioned isolated cells. Mean ±SD values relative to TBP mRNA are shown (n= 4). Significant differences to the respective untreated controls, are shown (*p< 0.05, unpaired t-test).

Journal: bioRxiv

Article Title: Chemokine profiling of melanoma-macrophage crosstalk identifies CCL8 and CCL15 as prognostic factors in cutaneous melanoma

doi: 10.1101/2023.10.04.560856

Figure Lengend Snippet: M1 and M2 macrophages were co-cultured with BLM melanoma cells for transcriptomic (24 h) and secretomic (72 h) analyses. (A) Gene set enrichment analyses (GSEA) comparing 24 hours exposed vs un-exposed isolated cells, as indicated (n=3 donors). Normalized Enrichment Score (NES) values from the main upregulated hallmark_pathwaysfor all groups,are shown. GOMF and KEGG gene sets were additionally studied for cytokine/ chemokine inflammatory pathways. False Discovery Rates are represented (FDR q value <0.01). (B) Representative scheme highlighting the coincident most upregulated secreted chemokines (fold >4 to both unex-posed macrophages and melanoma cells). (C) Secretomic analysis (38 chemokines) of 72 hours co-cultured supernatants comparing M1+ BLM or M2+BLM with unexposed macrophages (x-axis) or BLM (y-axis) cells. Fold logarithmic average changes are shown (n=4 donors). (D) CCL8 and CCL15 secretion assessed at 72 h macrophages ±BLM conditioned media. Mean ±standard deviation (SD) values are shown (n= 5 do-nors). (E) CCL8 and CCL15 mRNA expression levels in mutually conditioned isolated cells. Mean ±SD values relative to TBP mRNA are shown (n= 4). Significant differences to the respective untreated controls, are shown (*p< 0.05, unpaired t-test).

Article Snippet: Serum-deprived media ±recombinant human CCL8 or CCL15 (R&D Systems, Minnneapolis, MN) and ±5 μg/ml neutralizing antibodies for CCR1, CCR3 and CCR5 (supplementary material, Table S1) were added on top of the gels, and spheroids were allowed to invade for 72 hours.

Techniques: Cell Culture, Isolation, Standard Deviation, Expressing

(A) Serum deprivation survival assays of BLM, A375 and Skmel-103 melanoma cell lines in response to increasing concentra-tions of CCL8 and CCL15 chemokines (ng/ml), and to FCS 1%, as positive control. Mean ±SD optical density (OD) values, are shown (n= 4). (B) Proliferation response of melanoma cell lines to 200 ng/ml exogenous CCL8 and CCL15, and to FCS 1% as positive control. Mean ±SD percentages of BrdU+ nuclei, are shown (n= 3). (C) BLM spheroids embedded in 3D-collagen and allowed to invade for 72 h in the presence of increasing concentrations of exogenous CCL8 and CCL15, as indicated (ng/ml). Functional chemotactic axes were identified by using neutralizing antibodies against CCR1, CCR3, CCR5 and their corresponding control isotypes (5 μg/ml). Mean ±SD fold-invasion values, are shown (n= 3-6). Images show representative collagen-embedded spheroids showing basal and CCL15 stimulated invasion. Scale bar, 150 μm. (D) Immunoblots showing CCR1, CCR3 and CCR5 expression in whole-lysates of three melanoma cell lines and isolated CD14+ monocytes. (E) Serum deprivation survival and 3D-collagen invasion assays of monocytes in response to 100 ng/ml exogenous chemokines, including FCS 1%, as positive control (n= 5 donors). Significant differences to the respective untreated controls, are shown (*p< 0.05, paired t-test).

Journal: bioRxiv

Article Title: Chemokine profiling of melanoma-macrophage crosstalk identifies CCL8 and CCL15 as prognostic factors in cutaneous melanoma

doi: 10.1101/2023.10.04.560856

Figure Lengend Snippet: (A) Serum deprivation survival assays of BLM, A375 and Skmel-103 melanoma cell lines in response to increasing concentra-tions of CCL8 and CCL15 chemokines (ng/ml), and to FCS 1%, as positive control. Mean ±SD optical density (OD) values, are shown (n= 4). (B) Proliferation response of melanoma cell lines to 200 ng/ml exogenous CCL8 and CCL15, and to FCS 1% as positive control. Mean ±SD percentages of BrdU+ nuclei, are shown (n= 3). (C) BLM spheroids embedded in 3D-collagen and allowed to invade for 72 h in the presence of increasing concentrations of exogenous CCL8 and CCL15, as indicated (ng/ml). Functional chemotactic axes were identified by using neutralizing antibodies against CCR1, CCR3, CCR5 and their corresponding control isotypes (5 μg/ml). Mean ±SD fold-invasion values, are shown (n= 3-6). Images show representative collagen-embedded spheroids showing basal and CCL15 stimulated invasion. Scale bar, 150 μm. (D) Immunoblots showing CCR1, CCR3 and CCR5 expression in whole-lysates of three melanoma cell lines and isolated CD14+ monocytes. (E) Serum deprivation survival and 3D-collagen invasion assays of monocytes in response to 100 ng/ml exogenous chemokines, including FCS 1%, as positive control (n= 5 donors). Significant differences to the respective untreated controls, are shown (*p< 0.05, paired t-test).

Techniques: Positive Control, Functional Assay, Control, Western Blot, Expressing, Isolation

TAM (A) and tumor cell (B) average MFI of CCL15, CCL8, CCR1, CCR3 and CCR5 in non-metastasizing and metastasizing primary tumors.Mann-Whitney statistical analysis was used to compare non-metastasizing vs metastasizing melanomas; p-values are shown.(C) FFPE human melanoma samples stained for CD68 (TAM marker, red) and CCL15, CCL8, CCR1, CCR3 or CCR5 (green). Scale bar, 50 μm.

Journal: bioRxiv

Article Title: Chemokine profiling of melanoma-macrophage crosstalk identifies CCL8 and CCL15 as prognostic factors in cutaneous melanoma

doi: 10.1101/2023.10.04.560856

Figure Lengend Snippet: TAM (A) and tumor cell (B) average MFI of CCL15, CCL8, CCR1, CCR3 and CCR5 in non-metastasizing and metastasizing primary tumors.Mann-Whitney statistical analysis was used to compare non-metastasizing vs metastasizing melanomas; p-values are shown.(C) FFPE human melanoma samples stained for CD68 (TAM marker, red) and CCL15, CCL8, CCR1, CCR3 or CCR5 (green). Scale bar, 50 μm.

Techniques: MANN-WHITNEY, Staining, Marker

(A)Disease-free and overall survival 10-year Kaplan–Meier curves. Youden’s index was used to choose a cutoff point to classify the 67 primary melanomas as ‘low’ or ‘high’: TC CCL8 (MFI, 80 a.u.), TC CCL15 (98a.u.),TAM CCL15 (69 a.u.) and TAM CCR3 (78 a.u.). Log-rank p values, are shown. (B) Summarizing model, created with BioRender.com .

Journal: bioRxiv

Article Title: Chemokine profiling of melanoma-macrophage crosstalk identifies CCL8 and CCL15 as prognostic factors in cutaneous melanoma

doi: 10.1101/2023.10.04.560856

Figure Lengend Snippet: (A)Disease-free and overall survival 10-year Kaplan–Meier curves. Youden’s index was used to choose a cutoff point to classify the 67 primary melanomas as ‘low’ or ‘high’: TC CCL8 (MFI, 80 a.u.), TC CCL15 (98a.u.),TAM CCL15 (69 a.u.) and TAM CCR3 (78 a.u.). Log-rank p values, are shown. (B) Summarizing model, created with BioRender.com .

Techniques:

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1) Product Images from "Immune disease dialogue of chemokine-based cell communications as revealed by single-cell RNA sequencing meta-analysis"

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