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goat polyclonal antibody against human cxcl5 (R&D Systems)

Name: goat polyclonal antibody against human cxcl5
Brand: R&D Systems
Rating: 92 (13 reviews)

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R&D Systems goat polyclonal antibody against human cxcl5

Figure 3. Secreted <t>CXCL5</t> in the conditioned medium of the co-culture model with resistin-stimulated ADSCs promoted malignant behaviors of breast cancer cells. The isolated ADSCs were treated with resistin at 0 and 100 ng/ml (R0 and R100, respectively) for 48 h, followed by co-culture with MDA-MB-231 cells in the transwell model for another 72 h before the analyses in (A,B,F,G). (A) The conditioned medium from the co-culture of R-ADSCs (R100) or control ADSCs (R0) with MDA-MB-231 cells was collected and analyzed by cytokine/ chemokine proteome array. A total of 102 proteins were detected with duplicates for each protein. The position of CXCL5 on the array was highlighted. (B) Secreted protein level of CXCL5 in the conditioned medium from the co-culture of R-ADSCs (R100) or control ADSCs (R0) with MDA-MB-231 cells was analyzed by ELISA. (C) MDA-MB-231 cells treated with recombinant CXCL5 (0, 20, and 40 ng/ml) for 48 h were collected and evaluated by cell migration assay. (D) MDA-MB-231 cells treated with recombinant CXCL5 (0, 20, and 40 ng/ml) for 48 h were collected and evaluated by cell invasion assay. (E) MDA-MB-231 cells treated with recombinant CXCL5 (0, 20, and 40 ng/ml) for 48 h were collected and analyzed for the protein expression of mesenchymal marker Slug and cancer stemness marker Oct4 by Western blot. The original blot images in (A) and (E) were available in Supplementary Information. (F,G) CXCL5 neutralizing antibody was added ( +) or omitted (–) during the co-culture of R-ADSCs (R100) or control ADSCs (R0) with MDA-MB-231 cells. After the co-culture, MDA-MB-231 cells were collected and evaluated by cell migration assay in (F) and cell invasion assay in (G). Data were obtained from three independent experiments and presented as mean ± SEM. Statistical difference was determined by t-test comparing R100 group versus their corresponding R0 group as control, or comparing recombinant CXCL5 treatment group (20 and 40 ng/ml) versus recombinant CXCL5 control group (0 ng/ml). *p < 0.05; **p < 0.01; ***p < 0.001.

Goat Polyclonal Antibody Against Human Cxcl5, supplied by R&D Systems, used in various techniques. Bioz Stars score: 92/100, based on 13 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "ADSCs stimulated by resistin promote breast cancer cell malignancy via CXCL5 in a breast cancer coculture model."

Article Title: ADSCs stimulated by resistin promote breast cancer cell malignancy via CXCL5 in a breast cancer coculture model.

Journal: Scientific reports

doi: 10.1038/s41598-022-19290-6

Figure 3. Secreted CXCL5 in the conditioned medium of the co-culture model with resistin-stimulated ADSCs promoted malignant behaviors of breast cancer cells. The isolated ADSCs were treated with resistin at 0 and 100 ng/ml (R0 and R100, respectively) for 48 h, followed by co-culture with MDA-MB-231 cells in the transwell model for another 72 h before the analyses in (A,B,F,G). (A) The conditioned medium from the co-culture of R-ADSCs (R100) or control ADSCs (R0) with MDA-MB-231 cells was collected and analyzed by cytokine/ chemokine proteome array. A total of 102 proteins were detected with duplicates for each protein. The position of CXCL5 on the array was highlighted. (B) Secreted protein level of CXCL5 in the conditioned medium from the co-culture of R-ADSCs (R100) or control ADSCs (R0) with MDA-MB-231 cells was analyzed by ELISA. (C) MDA-MB-231 cells treated with recombinant CXCL5 (0, 20, and 40 ng/ml) for 48 h were collected and evaluated by cell migration assay. (D) MDA-MB-231 cells treated with recombinant CXCL5 (0, 20, and 40 ng/ml) for 48 h were collected and evaluated by cell invasion assay. (E) MDA-MB-231 cells treated with recombinant CXCL5 (0, 20, and 40 ng/ml) for 48 h were collected and analyzed for the protein expression of mesenchymal marker Slug and cancer stemness marker Oct4 by Western blot. The original blot images in (A) and (E) were available in Supplementary Information. (F,G) CXCL5 neutralizing antibody was added ( +) or omitted (–) during the co-culture of R-ADSCs (R100) or control ADSCs (R0) with MDA-MB-231 cells. After the co-culture, MDA-MB-231 cells were collected and evaluated by cell migration assay in (F) and cell invasion assay in (G). Data were obtained from three independent experiments and presented as mean ± SEM. Statistical difference was determined by t-test comparing R100 group versus their corresponding R0 group as control, or comparing recombinant CXCL5 treatment group (20 and 40 ng/ml) versus recombinant CXCL5 control group (0 ng/ml). *p < 0.05; **p < 0.01; ***p < 0.001.

Figure Legend Snippet: Figure 3. Secreted CXCL5 in the conditioned medium of the co-culture model with resistin-stimulated ADSCs promoted malignant behaviors of breast cancer cells. The isolated ADSCs were treated with resistin at 0 and 100 ng/ml (R0 and R100, respectively) for 48 h, followed by co-culture with MDA-MB-231 cells in the transwell model for another 72 h before the analyses in (A,B,F,G). (A) The conditioned medium from the co-culture of R-ADSCs (R100) or control ADSCs (R0) with MDA-MB-231 cells was collected and analyzed by cytokine/ chemokine proteome array. A total of 102 proteins were detected with duplicates for each protein. The position of CXCL5 on the array was highlighted. (B) Secreted protein level of CXCL5 in the conditioned medium from the co-culture of R-ADSCs (R100) or control ADSCs (R0) with MDA-MB-231 cells was analyzed by ELISA. (C) MDA-MB-231 cells treated with recombinant CXCL5 (0, 20, and 40 ng/ml) for 48 h were collected and evaluated by cell migration assay. (D) MDA-MB-231 cells treated with recombinant CXCL5 (0, 20, and 40 ng/ml) for 48 h were collected and evaluated by cell invasion assay. (E) MDA-MB-231 cells treated with recombinant CXCL5 (0, 20, and 40 ng/ml) for 48 h were collected and analyzed for the protein expression of mesenchymal marker Slug and cancer stemness marker Oct4 by Western blot. The original blot images in (A) and (E) were available in Supplementary Information. (F,G) CXCL5 neutralizing antibody was added ( +) or omitted (–) during the co-culture of R-ADSCs (R100) or control ADSCs (R0) with MDA-MB-231 cells. After the co-culture, MDA-MB-231 cells were collected and evaluated by cell migration assay in (F) and cell invasion assay in (G). Data were obtained from three independent experiments and presented as mean ± SEM. Statistical difference was determined by t-test comparing R100 group versus their corresponding R0 group as control, or comparing recombinant CXCL5 treatment group (20 and 40 ng/ml) versus recombinant CXCL5 control group (0 ng/ml). *p < 0.05; **p < 0.01; ***p < 0.001.

Techniques Used: Co-Culture Assay, Isolation, Control, Enzyme-linked Immunosorbent Assay, Recombinant, Cell Migration Assay, Invasion Assay, Expressing, Marker, Western Blot

Figure 5. Enhanced breast tumor growth and protein expression of CXCL5, Slug, and ERK phosphorylation in mice via xenograft of breast cancer cells after co-culture with resistin-stimulated ADSCs. The isolated ADSCs were treated with resistin at 0 and 50 ng/ml (denoted as R0 and R50, respectively) for 48 h, followed by co-culture with MDA-MB-231 cells in the transwell model for another 72 h. After the co-culture, MDA-MB-231 cells were collected and injected into the fourth mammary fat pads of female NOD/SCID mice for the following analyses. (A) The tumor volume, calculated by (width2 × length)/2, was measured weekly after palpable tumor mass was formed. (B) Upon sacrifice of the mice on week eight, the weight of individual tumor mass was measured. (C) The body weight of the mice was measured weekly. (D) The tumor mass was collected after sacrifice of the mice on week eight, and analyzed for CXCL5, Slug, and phospho-ERK1/2 protein expression by immunohistochemistry (IHC). The quantitative IHC scores were manually evaluated and calculated by multiplying the categorized percentage of stained cells (0, 0–24%; 1, 25‑49%; 2, 50‑74%; 3, 75‑100%) by the categorized intensity of staining (0, negative; 1, weak; 2, moderate; 3, strong). Data were obtained from three to six mice in each group and presented as mean ± SEM or box plots. Statistical difference was determined by t-test comparing R50 group versus R0 group as control. *p < 0.05; **p < 0.01; ***p < 0.001.

Figure Legend Snippet: Figure 5. Enhanced breast tumor growth and protein expression of CXCL5, Slug, and ERK phosphorylation in mice via xenograft of breast cancer cells after co-culture with resistin-stimulated ADSCs. The isolated ADSCs were treated with resistin at 0 and 50 ng/ml (denoted as R0 and R50, respectively) for 48 h, followed by co-culture with MDA-MB-231 cells in the transwell model for another 72 h. After the co-culture, MDA-MB-231 cells were collected and injected into the fourth mammary fat pads of female NOD/SCID mice for the following analyses. (A) The tumor volume, calculated by (width2 × length)/2, was measured weekly after palpable tumor mass was formed. (B) Upon sacrifice of the mice on week eight, the weight of individual tumor mass was measured. (C) The body weight of the mice was measured weekly. (D) The tumor mass was collected after sacrifice of the mice on week eight, and analyzed for CXCL5, Slug, and phospho-ERK1/2 protein expression by immunohistochemistry (IHC). The quantitative IHC scores were manually evaluated and calculated by multiplying the categorized percentage of stained cells (0, 0–24%; 1, 25‑49%; 2, 50‑74%; 3, 75‑100%) by the categorized intensity of staining (0, negative; 1, weak; 2, moderate; 3, strong). Data were obtained from three to six mice in each group and presented as mean ± SEM or box plots. Statistical difference was determined by t-test comparing R50 group versus R0 group as control. *p < 0.05; **p < 0.01; ***p < 0.001.

Techniques Used: Expressing, Phospho-proteomics, Co-Culture Assay, Isolation, Injection, Immunohistochemistry, Staining, Control

Figure 6. Correlation analysis for the protein expression of resistin, CXCL5, and ERK phosphorylation in the tumor and serum specimens from breast cancer patients. (A) Representative images of immunohistochemistry (IHC) staining for resistin, CXCL5, and phospho-ERK1/2 expression in breast tumor sections from breast cancer patients. (B–D) The quantitative IHC scores were evaluated by HistoQuest software, followed by Pearson correlation (r) analysis between resistin and CXCL5 in (B) (n = 96), resistin and phospho-ERK1/2 in (C) (n = 45), and CXCL5 and phospho-ERK1/2 in (D) (n = 45). (E) The serum levels of resistin and CXCL5 in breast cancer patients were determined by ELISA, followed by Pearson correlation (r) analysis (n = 120). The mean ± SD of resistin and CXCL5 was 31.4 ± 15.4 ng/ml and 707.9 ± 293.4 pg/ml, respectively. (F) Schematic summary of the current study. Our preclinical and clinical data together suggest that CXCL5 may be secreted by resistin-stimulated ADSCs in the breast tumor microenvironment, promoting breast cancer cell malignancy via the participation of ERK pathway and epithelial-to-mesenchymal transition. The schematic summary in (F) was produced using the illustration elements from Servier Medical Art (https://smart.servier.com), which is in compliance with the terms of the Creative Commons Attribution 3.0 Unported License (https://creativeco mmons.org/licenses/by/3.0/).

Figure Legend Snippet: Figure 6. Correlation analysis for the protein expression of resistin, CXCL5, and ERK phosphorylation in the tumor and serum specimens from breast cancer patients. (A) Representative images of immunohistochemistry (IHC) staining for resistin, CXCL5, and phospho-ERK1/2 expression in breast tumor sections from breast cancer patients. (B–D) The quantitative IHC scores were evaluated by HistoQuest software, followed by Pearson correlation (r) analysis between resistin and CXCL5 in (B) (n = 96), resistin and phospho-ERK1/2 in (C) (n = 45), and CXCL5 and phospho-ERK1/2 in (D) (n = 45). (E) The serum levels of resistin and CXCL5 in breast cancer patients were determined by ELISA, followed by Pearson correlation (r) analysis (n = 120). The mean ± SD of resistin and CXCL5 was 31.4 ± 15.4 ng/ml and 707.9 ± 293.4 pg/ml, respectively. (F) Schematic summary of the current study. Our preclinical and clinical data together suggest that CXCL5 may be secreted by resistin-stimulated ADSCs in the breast tumor microenvironment, promoting breast cancer cell malignancy via the participation of ERK pathway and epithelial-to-mesenchymal transition. The schematic summary in (F) was produced using the illustration elements from Servier Medical Art (https://smart.servier.com), which is in compliance with the terms of the Creative Commons Attribution 3.0 Unported License (https://creativeco mmons.org/licenses/by/3.0/).

Techniques Used: Expressing, Phospho-proteomics, Immunohistochemistry, Software, Enzyme-linked Immunosorbent Assay, Produced

Image Search Results

Journal: Scientific reports

Article Title: ADSCs stimulated by resistin promote breast cancer cell malignancy via CXCL5 in a breast cancer coculture model.

doi: 10.1038/s41598-022-19290-6

Figure Lengend Snippet: Figure 3. Secreted CXCL5 in the conditioned medium of the co-culture model with resistin-stimulated ADSCs promoted malignant behaviors of breast cancer cells. The isolated ADSCs were treated with resistin at 0 and 100 ng/ml (R0 and R100, respectively) for 48 h, followed by co-culture with MDA-MB-231 cells in the transwell model for another 72 h before the analyses in (A,B,F,G). (A) The conditioned medium from the co-culture of R-ADSCs (R100) or control ADSCs (R0) with MDA-MB-231 cells was collected and analyzed by cytokine/ chemokine proteome array. A total of 102 proteins were detected with duplicates for each protein. The position of CXCL5 on the array was highlighted. (B) Secreted protein level of CXCL5 in the conditioned medium from the co-culture of R-ADSCs (R100) or control ADSCs (R0) with MDA-MB-231 cells was analyzed by ELISA. (C) MDA-MB-231 cells treated with recombinant CXCL5 (0, 20, and 40 ng/ml) for 48 h were collected and evaluated by cell migration assay. (D) MDA-MB-231 cells treated with recombinant CXCL5 (0, 20, and 40 ng/ml) for 48 h were collected and evaluated by cell invasion assay. (E) MDA-MB-231 cells treated with recombinant CXCL5 (0, 20, and 40 ng/ml) for 48 h were collected and analyzed for the protein expression of mesenchymal marker Slug and cancer stemness marker Oct4 by Western blot. The original blot images in (A) and (E) were available in Supplementary Information. (F,G) CXCL5 neutralizing antibody was added ( +) or omitted (–) during the co-culture of R-ADSCs (R100) or control ADSCs (R0) with MDA-MB-231 cells. After the co-culture, MDA-MB-231 cells were collected and evaluated by cell migration assay in (F) and cell invasion assay in (G). Data were obtained from three independent experiments and presented as mean ± SEM. Statistical difference was determined by t-test comparing R100 group versus their corresponding R0 group as control, or comparing recombinant CXCL5 treatment group (20 and 40 ng/ml) versus recombinant CXCL5 control group (0 ng/ml). *p < 0.05; **p < 0.01; ***p < 0.001.

Article Snippet: The primary antibodies used in this study for IHC are listed as follows: rabbit polyclonal antibody against human Slug (GeneTex, Hsinchu, Taiwan); goat polyclonal antibody against human CXCL5 (R&D Systems, Minneapolis, MN, USA); mouse monoclonal antibody against human resistin (clone C-10; Santa Cruz Biotechnology, Dallas, TX, USA); rabbit monoclonal antibody against human phosphorylated ERK1/2 at Thr202/Tyr204 (clone D13.14.4E; Cell Signaling Technology, Danvers, MA, USA).

Techniques: Co-Culture Assay, Isolation, Control, Enzyme-linked Immunosorbent Assay, Recombinant, Cell Migration Assay, Invasion Assay, Expressing, Marker, Western Blot

Journal: Scientific reports

Article Title: ADSCs stimulated by resistin promote breast cancer cell malignancy via CXCL5 in a breast cancer coculture model.

doi: 10.1038/s41598-022-19290-6

Figure Lengend Snippet: Figure 5. Enhanced breast tumor growth and protein expression of CXCL5, Slug, and ERK phosphorylation in mice via xenograft of breast cancer cells after co-culture with resistin-stimulated ADSCs. The isolated ADSCs were treated with resistin at 0 and 50 ng/ml (denoted as R0 and R50, respectively) for 48 h, followed by co-culture with MDA-MB-231 cells in the transwell model for another 72 h. After the co-culture, MDA-MB-231 cells were collected and injected into the fourth mammary fat pads of female NOD/SCID mice for the following analyses. (A) The tumor volume, calculated by (width2 × length)/2, was measured weekly after palpable tumor mass was formed. (B) Upon sacrifice of the mice on week eight, the weight of individual tumor mass was measured. (C) The body weight of the mice was measured weekly. (D) The tumor mass was collected after sacrifice of the mice on week eight, and analyzed for CXCL5, Slug, and phospho-ERK1/2 protein expression by immunohistochemistry (IHC). The quantitative IHC scores were manually evaluated and calculated by multiplying the categorized percentage of stained cells (0, 0–24%; 1, 25‑49%; 2, 50‑74%; 3, 75‑100%) by the categorized intensity of staining (0, negative; 1, weak; 2, moderate; 3, strong). Data were obtained from three to six mice in each group and presented as mean ± SEM or box plots. Statistical difference was determined by t-test comparing R50 group versus R0 group as control. *p < 0.05; **p < 0.01; ***p < 0.001.

Techniques: Expressing, Phospho-proteomics, Co-Culture Assay, Isolation, Injection, Immunohistochemistry, Staining, Control

Journal: Scientific reports

Article Title: ADSCs stimulated by resistin promote breast cancer cell malignancy via CXCL5 in a breast cancer coculture model.

doi: 10.1038/s41598-022-19290-6

Figure Lengend Snippet: Figure 6. Correlation analysis for the protein expression of resistin, CXCL5, and ERK phosphorylation in the tumor and serum specimens from breast cancer patients. (A) Representative images of immunohistochemistry (IHC) staining for resistin, CXCL5, and phospho-ERK1/2 expression in breast tumor sections from breast cancer patients. (B–D) The quantitative IHC scores were evaluated by HistoQuest software, followed by Pearson correlation (r) analysis between resistin and CXCL5 in (B) (n = 96), resistin and phospho-ERK1/2 in (C) (n = 45), and CXCL5 and phospho-ERK1/2 in (D) (n = 45). (E) The serum levels of resistin and CXCL5 in breast cancer patients were determined by ELISA, followed by Pearson correlation (r) analysis (n = 120). The mean ± SD of resistin and CXCL5 was 31.4 ± 15.4 ng/ml and 707.9 ± 293.4 pg/ml, respectively. (F) Schematic summary of the current study. Our preclinical and clinical data together suggest that CXCL5 may be secreted by resistin-stimulated ADSCs in the breast tumor microenvironment, promoting breast cancer cell malignancy via the participation of ERK pathway and epithelial-to-mesenchymal transition. The schematic summary in (F) was produced using the illustration elements from Servier Medical Art (https://smart.servier.com), which is in compliance with the terms of the Creative Commons Attribution 3.0 Unported License (https://creativeco mmons.org/licenses/by/3.0/).

Techniques: Expressing, Phospho-proteomics, Immunohistochemistry, Software, Enzyme-linked Immunosorbent Assay, Produced

CCL20/CCR6 mRNA expression in pancreatic diseases . Gene expression of [A] CCL20 and [B] CCR6 in chronic pancreatitis (CP, n = 22), pancreatic cystadenomas (PA, n = 11), pancreatic carcinoma (PCA, n = 25) compared to matched normal pancreatic tissues as determined by Q-RT-PCR. Q-RT-PCR data are expressed as mean +/- SEM, *P < 0.05. Fold increase above 1 indicates CCL20/CCR6 up-regulation compared to normal tissues.

Journal: Journal of Translational Medicine

Article Title: CCL20/CCR6 expression profile in pancreatic cancer

doi: 10.1186/1479-5876-8-45

Figure Lengend Snippet: CCL20/CCR6 mRNA expression in pancreatic diseases . Gene expression of [A] CCL20 and [B] CCR6 in chronic pancreatitis (CP, n = 22), pancreatic cystadenomas (PA, n = 11), pancreatic carcinoma (PCA, n = 25) compared to matched normal pancreatic tissues as determined by Q-RT-PCR. Q-RT-PCR data are expressed as mean +/- SEM, *P < 0.05. Fold increase above 1 indicates CCL20/CCR6 up-regulation compared to normal tissues.

Article Snippet: Overnight incubation at 4°C with primary goat polyclonal anti-human CCL20 antibody (15 μg/ml, AF254, R&D Systems, Minneapolis, Minn., USA) was followed by incubation of secondary biotinylated rabbit anti-goat IgG antibody and the avidin-biotin-peroxidase reaction (Vectastain ABC ELITE Kit, Vector Laboratories, Burlingame, CA, USA).

Techniques: Expressing, Gene Expression, Reverse Transcription Polymerase Chain Reaction

CCL20/CCR6 protein expression in pancreatic diseases . [A] CCL20 protein concentrations (pg/ml pro mg total protein) in chronic pancreatitis (CP, n = 22), pancreatic cystadenomas (PA, n = 11), pancreatic carcinoma (PCA, n = 25) compared to the matched normal pancreatic tissue levels (mean ± SEM), * p < 0.05. [B] Expression of chemokine receptor CCR6 in CP, PA and PCA as determined by Western blot analysis. Total cell lysates of tumor tissues of representative patients of each disease entity were immunoblotted with antibodies specifically recognizing chemokine receptor CCR6. Acute leukemia cell line HL60 served as a positive control for the detection of CCR6. Quantification has been performed using image J software * p < 0.05.

Journal: Journal of Translational Medicine

Article Title: CCL20/CCR6 expression profile in pancreatic cancer

doi: 10.1186/1479-5876-8-45

Figure Lengend Snippet: CCL20/CCR6 protein expression in pancreatic diseases . [A] CCL20 protein concentrations (pg/ml pro mg total protein) in chronic pancreatitis (CP, n = 22), pancreatic cystadenomas (PA, n = 11), pancreatic carcinoma (PCA, n = 25) compared to the matched normal pancreatic tissue levels (mean ± SEM), * p < 0.05. [B] Expression of chemokine receptor CCR6 in CP, PA and PCA as determined by Western blot analysis. Total cell lysates of tumor tissues of representative patients of each disease entity were immunoblotted with antibodies specifically recognizing chemokine receptor CCR6. Acute leukemia cell line HL60 served as a positive control for the detection of CCR6. Quantification has been performed using image J software * p < 0.05.

Techniques: Expressing, Western Blot, Positive Control, Software

Results of anti-CCL20 immunohistochemistry in normal and diseased pancreatic tissues . Representative example of CCL20 expression in [A,B] pancreatic islet cells and epithelial cells of pancreatic ducts, [C] necrotic parenchyma and epithelial cells of pancreatic ducts in chronic pancreatitis tissues [D] epithelial cells of the characteristic net-like structures of pancreatic cystadenoma [E,F] cytoplasms of ductal epithelial cancer cells and in infiltrates of perineural sheaths. Anti-CCL20 goat anti-human, 75 μg/ml (MIP-3α; R&D Systems; Minneapolis, MN, USA. Avidin Biotin Complex (ABC) Method. (original magnification: × 200 and 400, respectively).

Journal: Journal of Translational Medicine

Article Title: CCL20/CCR6 expression profile in pancreatic cancer

doi: 10.1186/1479-5876-8-45

Figure Lengend Snippet: Results of anti-CCL20 immunohistochemistry in normal and diseased pancreatic tissues . Representative example of CCL20 expression in [A,B] pancreatic islet cells and epithelial cells of pancreatic ducts, [C] necrotic parenchyma and epithelial cells of pancreatic ducts in chronic pancreatitis tissues [D] epithelial cells of the characteristic net-like structures of pancreatic cystadenoma [E,F] cytoplasms of ductal epithelial cancer cells and in infiltrates of perineural sheaths. Anti-CCL20 goat anti-human, 75 μg/ml (MIP-3α; R&D Systems; Minneapolis, MN, USA. Avidin Biotin Complex (ABC) Method. (original magnification: × 200 and 400, respectively).

Techniques: Immunohistochemistry, Expressing, Avidin-Biotin Assay

Expression of CCL20 in different tumor categories of PCA as determined by [A] Q-RT-PCR and [B] ELISA . mRNA and protein expression profiles of CCL20 (pg/ml pro mg total protein) were measured in PCA tissues and matched normal tissues in pT1 + pT2 (n = 11) (A) and pT3 + pT4 (n = 14) (B), respectively. For Q-RT-PCR data fold increase above 1 indicates CCL20 up-regulation in PCA compared to normal tissues. All data are expressed as mean ± SEM, * p < 0.05

Journal: Journal of Translational Medicine

Article Title: CCL20/CCR6 expression profile in pancreatic cancer

doi: 10.1186/1479-5876-8-45

Figure Lengend Snippet: Expression of CCL20 in different tumor categories of PCA as determined by [A] Q-RT-PCR and [B] ELISA . mRNA and protein expression profiles of CCL20 (pg/ml pro mg total protein) were measured in PCA tissues and matched normal tissues in pT1 + pT2 (n = 11) (A) and pT3 + pT4 (n = 14) (B), respectively. For Q-RT-PCR data fold increase above 1 indicates CCL20 up-regulation in PCA compared to normal tissues. All data are expressed as mean ± SEM, * p < 0.05

Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay

Protein array analyses were conduced by testing the cell culture supernatants of FB-PDGF-B/Ad5 versus FB-LacZ/Ad5 using a protein array set of RayBio® Human Angiogenesis Antibody Array I kit. CXCL5 (ENA-78) and bFGF were elevated 8-fold and 5-fold in the PDGF-B-aFB group, respectively, compared to the control fibroblast group. Expression of IFN-γ, RANTES and thrombopoietin (ThBo) was slightly decreased. Experiments were repeated three times, independently. Means ± SD were analyzed by ANOVA or student t-test.

Journal:

Article Title: A CXCL5- and bFGF-Dependent Effect of PDGF-B-Activated Fibroblasts in Promoting Trafficking and Differentiation of Bone Marrow-Derived Mesenchymal Stem Cells

doi: 10.1016/j.yexcr.2008.04.007

Figure Lengend Snippet: Protein array analyses were conduced by testing the cell culture supernatants of FB-PDGF-B/Ad5 versus FB-LacZ/Ad5 using a protein array set of RayBio® Human Angiogenesis Antibody Array I kit. CXCL5 (ENA-78) and bFGF were elevated 8-fold and 5-fold in the PDGF-B-aFB group, respectively, compared to the control fibroblast group. Expression of IFN-γ, RANTES and thrombopoietin (ThBo) was slightly decreased. Experiments were repeated three times, independently. Means ± SD were analyzed by ANOVA or student t-test.

Article Snippet: Goat anti-human PDGF-B antibody, goat anti-human CXCL5 (ENA-78) antibody, rabbit anti-human bFGF, and isotype matched control antibodies were purchased from R&D Systems.

Techniques: Protein Array, Cell Culture, Ab Array, Control, Expressing

(A) Inhibition of BM-MSC invasion/migration by blocking antibodies against PDGF-B, CXCL5 and bFGF. Effects of blocking antibodies against PDGF-B, CXCL5 or bFGF on BM-MSC migration/invasion in 3D gel. Average percent of GFP+-BM-MSCs per HPF in the presence of FB-LacZ/Ad5 versus FB-PDGF-B/Ad5. Invasion/migration of BM-MSCs into collagen gels was significantly suppressed (**P<0.05). When recombinant PDGF-B or blocking antibodies were used in the collagen, they were added to the medium at the same concentration. Concentration of blocking antibody was within its neutralization dose (ND50), as titrated by the manufacturer, R&D Systems. All experiments were performed in duplicate and repeated three times, independently. Means ± SD were analyzed by ANOVA or student t-test. (B) Representative sections under 20X magnification were shown (order from left to right is the same as the bar graph). (C) Effect of exogenous CXCL5 and/or bFGF on BM-MSC invasion/migration into 3D gels. Invaded cell number of GFP+-BM-MSCs per HPF in the 3D gels in which FBs were not activated by PDGF-B was shown. CXCL5 and/or bFGF significantly promoted invasion/migration of BM-MSCs into 3D collagen gels compared with non-stimulated (−) group. Data were normalized by comparison with hrPDGF-B groups which were set as “100”. All experiments were performed in duplicate and repeated three times, independently. Means ± SD were analyzed by ANOVA or student t-test.

Journal:

Article Title: A CXCL5- and bFGF-Dependent Effect of PDGF-B-Activated Fibroblasts in Promoting Trafficking and Differentiation of Bone Marrow-Derived Mesenchymal Stem Cells

doi: 10.1016/j.yexcr.2008.04.007

Figure Lengend Snippet: (A) Inhibition of BM-MSC invasion/migration by blocking antibodies against PDGF-B, CXCL5 and bFGF. Effects of blocking antibodies against PDGF-B, CXCL5 or bFGF on BM-MSC migration/invasion in 3D gel. Average percent of GFP+-BM-MSCs per HPF in the presence of FB-LacZ/Ad5 versus FB-PDGF-B/Ad5. Invasion/migration of BM-MSCs into collagen gels was significantly suppressed (**P<0.05). When recombinant PDGF-B or blocking antibodies were used in the collagen, they were added to the medium at the same concentration. Concentration of blocking antibody was within its neutralization dose (ND50), as titrated by the manufacturer, R&D Systems. All experiments were performed in duplicate and repeated three times, independently. Means ± SD were analyzed by ANOVA or student t-test. (B) Representative sections under 20X magnification were shown (order from left to right is the same as the bar graph). (C) Effect of exogenous CXCL5 and/or bFGF on BM-MSC invasion/migration into 3D gels. Invaded cell number of GFP+-BM-MSCs per HPF in the 3D gels in which FBs were not activated by PDGF-B was shown. CXCL5 and/or bFGF significantly promoted invasion/migration of BM-MSCs into 3D collagen gels compared with non-stimulated (−) group. Data were normalized by comparison with hrPDGF-B groups which were set as “100”. All experiments were performed in duplicate and repeated three times, independently. Means ± SD were analyzed by ANOVA or student t-test.

Article Snippet: Goat anti-human PDGF-B antibody, goat anti-human CXCL5 (ENA-78) antibody, rabbit anti-human bFGF, and isotype matched control antibodies were purchased from R&D Systems.

Techniques: Inhibition, Migration, Blocking Assay, Recombinant, Concentration Assay, Neutralization, Comparison

(A) The effects of blocking antibodies against PDGF-B, CXCL5 or bFGF on myofibroblast differentiation of BM-MSCs in 3D gel. Average percentage of α-SMA+-BM-MSCs per HPF in 3D assays with FB-LacZ/Ad5 versus FB-PDGF-B/Ad5, respectively, under treatment with neutralization antibodies against PDGF-B, CXCL5 or bFGF. See Fig 3A for the control. A partial, but significant inhibition of differentiation was observed. Concentration of blocking antibody was within its neutralization dose (ND50), as titrated by the manufacturer, R&D Systems. All experiments were performed in duplicate and repeated three times, independently. Means ± SD were analyzed by ANOVA or student t-test. (B) Representative sections under 20X magnification were shown (see Fig 3B for the control).

Journal:

Article Title: A CXCL5- and bFGF-Dependent Effect of PDGF-B-Activated Fibroblasts in Promoting Trafficking and Differentiation of Bone Marrow-Derived Mesenchymal Stem Cells

doi: 10.1016/j.yexcr.2008.04.007

Figure Lengend Snippet: (A) The effects of blocking antibodies against PDGF-B, CXCL5 or bFGF on myofibroblast differentiation of BM-MSCs in 3D gel. Average percentage of α-SMA+-BM-MSCs per HPF in 3D assays with FB-LacZ/Ad5 versus FB-PDGF-B/Ad5, respectively, under treatment with neutralization antibodies against PDGF-B, CXCL5 or bFGF. See Fig 3A for the control. A partial, but significant inhibition of differentiation was observed. Concentration of blocking antibody was within its neutralization dose (ND50), as titrated by the manufacturer, R&D Systems. All experiments were performed in duplicate and repeated three times, independently. Means ± SD were analyzed by ANOVA or student t-test. (B) Representative sections under 20X magnification were shown (see Fig 3B for the control).

Article Snippet: Goat anti-human PDGF-B antibody, goat anti-human CXCL5 (ENA-78) antibody, rabbit anti-human bFGF, and isotype matched control antibodies were purchased from R&D Systems.

Techniques: Blocking Assay, Neutralization, Control, Inhibition, Concentration Assay

Expression of (A) CXCL1, (B) CXCL5 and (C) CXCL6 in different tumor categories of colorectal carcinoma (CRC) as determined by Q-RT-PCR . Q-RT-PCR data are expressed as mean +/- standard error of the mean (SEM), * P < 0.05, ** P < 0.001, n = 23 and 25, respectively. Fold increase above 1 indicates chemokine overexpression in CRC tissues related to unaffected neighbor tissues, respectively. Note the different scale for CXCL1, CXCL5 and CXCL6 expression.

Journal: BMC Cancer

Article Title: ELR+ CXC chemokine expression in benign and malignant colorectal conditions

doi: 10.1186/1471-2407-8-178

Figure Lengend Snippet: Expression of (A) CXCL1, (B) CXCL5 and (C) CXCL6 in different tumor categories of colorectal carcinoma (CRC) as determined by Q-RT-PCR . Q-RT-PCR data are expressed as mean +/- standard error of the mean (SEM), * P < 0.05, ** P < 0.001, n = 23 and 25, respectively. Fold increase above 1 indicates chemokine overexpression in CRC tissues related to unaffected neighbor tissues, respectively. Note the different scale for CXCL1, CXCL5 and CXCL6 expression.

Article Snippet: Overnight incubation at 4°C with primary goat polyclonal anti-human CXCL5 antibody (15 μg/ml, AF254, R&D Systems, Minneapolis, Minn., USA) or primary goat anti-human CXCL1 antibody (3.5 μg/ml, sc-1374, Santa Cruz Biotechnology, Santa Cruz, Calif., USA) was followed by incubation of secondary biotinylated biotinylated rabbit anti-goat IgG antibody and the avidin-biotin-peroxidase reaction (Vectastain ABC ELITE Kit, Vector Laboratories, Burlingame, CA, USA).

Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction, Over Expression

Expression of CXCL1, CXCL5 and CXCL6 in colorectal liver metastases (CRLM) and corresponding primary colorectal tumors as determined by Q-RT-PCR . Q-RT-PCR data are expressed as mean +/- standard error of the mean (SEM), * P < 0.05, ** P < 0.001, n = 16 and 14, respectively. Fold increase above 1 indicates chemokine overexpression in affected tissues related to unaffected neighbor tissues, respectively.

Journal: BMC Cancer

Article Title: ELR+ CXC chemokine expression in benign and malignant colorectal conditions

doi: 10.1186/1471-2407-8-178

Figure Lengend Snippet: Expression of CXCL1, CXCL5 and CXCL6 in colorectal liver metastases (CRLM) and corresponding primary colorectal tumors as determined by Q-RT-PCR . Q-RT-PCR data are expressed as mean +/- standard error of the mean (SEM), * P < 0.05, ** P < 0.001, n = 16 and 14, respectively. Fold increase above 1 indicates chemokine overexpression in affected tissues related to unaffected neighbor tissues, respectively.

Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction, Over Expression

Expression of (A) CXCL1, (B) CXCL5 and (C) CXCL6 in colorectal adenoma (CRA) and colorectal carcinoma (CRC) tissue specimens as determined by ELISA assays . Elisa results are presented as absolute values of pg per ml chemokine ligand per mg total protein in CRA and CRC tissues and unaffected neighbor tissues, respectively. The data are expressed as mean +/- standard error of the mean (SEM), * P < 0.05, ** P < 0.001, n = 30 and 48, respectively. Note the different scale for CXCL1, CXCL5 and CXCL6 expression.

Journal: BMC Cancer

Article Title: ELR+ CXC chemokine expression in benign and malignant colorectal conditions

doi: 10.1186/1471-2407-8-178

Figure Lengend Snippet: Expression of (A) CXCL1, (B) CXCL5 and (C) CXCL6 in colorectal adenoma (CRA) and colorectal carcinoma (CRC) tissue specimens as determined by ELISA assays . Elisa results are presented as absolute values of pg per ml chemokine ligand per mg total protein in CRA and CRC tissues and unaffected neighbor tissues, respectively. The data are expressed as mean +/- standard error of the mean (SEM), * P < 0.05, ** P < 0.001, n = 30 and 48, respectively. Note the different scale for CXCL1, CXCL5 and CXCL6 expression.

Techniques: Expressing, Enzyme-linked Immunosorbent Assay

Expression of CXCL1 and CXCL5 and in (A) colorectal carcinoma (CRC) and (B) colorectal adenoma (CRA) tissue specimens as determined by ELISA assays . Elisa results are presented as absolute values of pg per ml chemokine ligand per mg total protein in CRC and CRA tissues and unaffected neighbor tissues, respectively. The data are expressed as mean +/- standard error of the mean (SEM), * P < 0.05, ** P < 0.001, n = 48 and 30, respectively.

Journal: BMC Cancer

Article Title: ELR+ CXC chemokine expression in benign and malignant colorectal conditions

doi: 10.1186/1471-2407-8-178

Figure Lengend Snippet: Expression of CXCL1 and CXCL5 and in (A) colorectal carcinoma (CRC) and (B) colorectal adenoma (CRA) tissue specimens as determined by ELISA assays . Elisa results are presented as absolute values of pg per ml chemokine ligand per mg total protein in CRC and CRA tissues and unaffected neighbor tissues, respectively. The data are expressed as mean +/- standard error of the mean (SEM), * P < 0.05, ** P < 0.001, n = 48 and 30, respectively.

Techniques: Expressing, Enzyme-linked Immunosorbent Assay

Detection of CXCL5 protein expression in representative CRA, CRC and CRLM specimens as assessed by immunohistochemical staining with CXCL5 -specific antibodies . (A) Weak cytoplasmic signals in basal crypt cells within tumor neighbor tissues of CRA, (B) very weak immunostaining in CRA specimens, (C) weak insular epithelial signals in tumor neighbor tissues of CRC, (D) intense basal and apical epithelial signals and interspersed rare mesenchymal signals in CRC tissues, (E) no substantial reactivity in corresponding neighbour tissues of CRLM and (F) intensive staining signals in epithelial and mesenchymal cells within tumor areas of CRLM specimens (original magnification 200 and 400 fold, respectively).

Journal: BMC Cancer

Article Title: ELR+ CXC chemokine expression in benign and malignant colorectal conditions

doi: 10.1186/1471-2407-8-178

Figure Lengend Snippet: Detection of CXCL5 protein expression in representative CRA, CRC and CRLM specimens as assessed by immunohistochemical staining with CXCL5 -specific antibodies . (A) Weak cytoplasmic signals in basal crypt cells within tumor neighbor tissues of CRA, (B) very weak immunostaining in CRA specimens, (C) weak insular epithelial signals in tumor neighbor tissues of CRC, (D) intense basal and apical epithelial signals and interspersed rare mesenchymal signals in CRC tissues, (E) no substantial reactivity in corresponding neighbour tissues of CRLM and (F) intensive staining signals in epithelial and mesenchymal cells within tumor areas of CRLM specimens (original magnification 200 and 400 fold, respectively).

Techniques: Expressing, Immunohistochemical staining, Staining, Immunostaining

Figure 1. Plasma CXCL5 concentrations in healthy controls and colorectal cancer (CRC) patients. CRC patients have significantly lower concentrations compared with controls.

Journal: International Journal of Oncology

Article Title: Expression and gene polymorphisms of the chemokine CXCL5 in colorectal cancer patients

doi: 10.3892/ijo.31.1.97

Figure Lengend Snippet: Figure 1. Plasma CXCL5 concentrations in healthy controls and colorectal cancer (CRC) patients. CRC patients have significantly lower concentrations compared with controls.

Article Snippet: Sections were subsequently incubated with a primary goat anti-human polyclonal CXCL5 antibody (R&D Systems Europe) in appropriate dilution overnight at 4 ̊C.

Techniques: Clinical Proteomics

Figure 3. Images of immunohistochemical staining of CXCL5 in cancer and normal tissue from patients with colorectal cancer. CXCL5 protein expression is present in cancer (A) and in normal (B) epithelial cells. Control staining of normal tissue (C) with only the secondary antibody, demonstrating the specificity of the primary antibody.

Journal: International Journal of Oncology

Article Title: Expression and gene polymorphisms of the chemokine CXCL5 in colorectal cancer patients

doi: 10.3892/ijo.31.1.97

Figure Lengend Snippet: Figure 3. Images of immunohistochemical staining of CXCL5 in cancer and normal tissue from patients with colorectal cancer. CXCL5 protein expression is present in cancer (A) and in normal (B) epithelial cells. Control staining of normal tissue (C) with only the secondary antibody, demonstrating the specificity of the primary antibody.

Article Snippet: Sections were subsequently incubated with a primary goat anti-human polyclonal CXCL5 antibody (R&D Systems Europe) in appropriate dilution overnight at 4 ̊C.

Techniques: Immunohistochemical staining, Staining, Expressing, Control

Figure 4. Correlation between IL-1ß and CXCL5 concentrations in the cancer tissue from CRC patients (n=48).

Journal: International Journal of Oncology

Article Title: Expression and gene polymorphisms of the chemokine CXCL5 in colorectal cancer patients

doi: 10.3892/ijo.31.1.97

Figure Lengend Snippet: Figure 4. Correlation between IL-1ß and CXCL5 concentrations in the cancer tissue from CRC patients (n=48).

Article Snippet: Sections were subsequently incubated with a primary goat anti-human polyclonal CXCL5 antibody (R&D Systems Europe) in appropriate dilution overnight at 4 ̊C.

Techniques:

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1) Product Images from "ADSCs stimulated by resistin promote breast cancer cell malignancy via CXCL5 in a breast cancer coculture model."

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