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il8 neutralizing antibody  (Becton Dickinson)

 
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    Becton Dickinson il8 neutralizing antibody
    A Representative images of H&E staining and CD10/GPR77 immunofluorescent staining in serial sections of the pre-treatment breast cancer biopsies of chemosensitive ( n = 3) and chemoresistant ( n = 3) patients. B , C Western blotting ( B ) for α-SMA, FAP, CD10, and GPR77 and flow cytometric analysis ( C ) for CD10 and GPR77 in primary normal breast fibroblasts (NBFs) treated with pre-treatment tumor conditional medium (CM). D Cytokine arrays of pre-treatment tumor CM, squares indicate the cytokines with significant changes. E Signal intensity of indicated cytokines in the cytokine arrays and their relative fold change between the chemoresistant ( n = 3) and chemosensitive tumors ( n = 3) F Flow cytometric analysis for CD10 and GPR77 in NBFs treated with chemosensitive or chemoresistant tumor CM added without or with neutralizing antibodies against IL6(αIL6), <t>IL8(αIL8)</t> or CCL18(αCCL18). The patients with complete remission (CR) or partial remission (PR) were classified as chemosensitive, while those with stable disease (SD) or progressive disease (PD) were chemoresistant.
    Il8 Neutralizing Antibody, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/il8+neutralizing+antibody/il6+neutralizing+antibody/pmc09836934-251-16-21
    Average 90 stars, based on 1 article reviews
    il8 neutralizing antibody - by Bioz Stars, 2026-11
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    Images

    1) Product Images from "CCL18 signaling from tumor-associated macrophages activates fibroblasts to adopt a chemoresistance-inducing phenotype"

    Article Title: CCL18 signaling from tumor-associated macrophages activates fibroblasts to adopt a chemoresistance-inducing phenotype

    Journal: Oncogene

    doi: 10.1038/s41388-022-02540-2

    A Representative images of H&E staining and CD10/GPR77 immunofluorescent staining in serial sections of the pre-treatment breast cancer biopsies of chemosensitive ( n = 3) and chemoresistant ( n = 3) patients. B , C Western blotting ( B ) for α-SMA, FAP, CD10, and GPR77 and flow cytometric analysis ( C ) for CD10 and GPR77 in primary normal breast fibroblasts (NBFs) treated with pre-treatment tumor conditional medium (CM). D Cytokine arrays of pre-treatment tumor CM, squares indicate the cytokines with significant changes. E Signal intensity of indicated cytokines in the cytokine arrays and their relative fold change between the chemoresistant ( n = 3) and chemosensitive tumors ( n = 3) F Flow cytometric analysis for CD10 and GPR77 in NBFs treated with chemosensitive or chemoresistant tumor CM added without or with neutralizing antibodies against IL6(αIL6), IL8(αIL8) or CCL18(αCCL18). The patients with complete remission (CR) or partial remission (PR) were classified as chemosensitive, while those with stable disease (SD) or progressive disease (PD) were chemoresistant.
    Figure Legend Snippet: A Representative images of H&E staining and CD10/GPR77 immunofluorescent staining in serial sections of the pre-treatment breast cancer biopsies of chemosensitive ( n = 3) and chemoresistant ( n = 3) patients. B , C Western blotting ( B ) for α-SMA, FAP, CD10, and GPR77 and flow cytometric analysis ( C ) for CD10 and GPR77 in primary normal breast fibroblasts (NBFs) treated with pre-treatment tumor conditional medium (CM). D Cytokine arrays of pre-treatment tumor CM, squares indicate the cytokines with significant changes. E Signal intensity of indicated cytokines in the cytokine arrays and their relative fold change between the chemoresistant ( n = 3) and chemosensitive tumors ( n = 3) F Flow cytometric analysis for CD10 and GPR77 in NBFs treated with chemosensitive or chemoresistant tumor CM added without or with neutralizing antibodies against IL6(αIL6), IL8(αIL8) or CCL18(αCCL18). The patients with complete remission (CR) or partial remission (PR) were classified as chemosensitive, while those with stable disease (SD) or progressive disease (PD) were chemoresistant.

    Techniques Used: Staining, Western Blot

    A The growth inhibition rate of docetaxel (up) and cisplatin (down) on MCF-7, BT474 or BT549 cultured alone (Ctrl) or co-cultured with NBFs underwent indicated treatment ( n = 3). B The growth inhibition rate of docetaxel on MCF-7 (up) and SK-BR3 (down) cells cultured alone (Ctrl) or co-cultured with NBFs underwent indicated treatment ( n = 3). C , D Representative western blotting ( C ) and quantification ( D ) for cleavage of caspase-3 and PARP in SK-BR3 cells cultured alone (Ctrl) or co-cultured with NBFs underwent indicated treatment and challenged with cisplatin ( n = 3). E , F The percentage of CD44 + CD24 - ( E ) and ALDH1 + ( F ) cells in MCF-7 cells cultured alone (UT) or co-cultured with NBFs underwent indicated treatment. G – I The apoptosis after cisplatin treatment ( G ), the ALDH1 + ( H ) and the CD44 + CD24 - ( I ) proportion of MCF-7 cells cultured alone or co-cultured with untreated or CCL18-treated NBFs transduced with GFP shRNA or IL-6 and IL-8 shRNA ( n = 3). Data expressed as mean ± SEM, *** P < 0.001 compared with NBFs co-cultured with untreated TAMs ( A ), untreated NBFs ( B , D – F ) or CCL18-treated NBFs without shRNA transduction ( G – I ) by two-tailed one-way ANOVA with Dunnett’s multiple comparison test.
    Figure Legend Snippet: A The growth inhibition rate of docetaxel (up) and cisplatin (down) on MCF-7, BT474 or BT549 cultured alone (Ctrl) or co-cultured with NBFs underwent indicated treatment ( n = 3). B The growth inhibition rate of docetaxel on MCF-7 (up) and SK-BR3 (down) cells cultured alone (Ctrl) or co-cultured with NBFs underwent indicated treatment ( n = 3). C , D Representative western blotting ( C ) and quantification ( D ) for cleavage of caspase-3 and PARP in SK-BR3 cells cultured alone (Ctrl) or co-cultured with NBFs underwent indicated treatment and challenged with cisplatin ( n = 3). E , F The percentage of CD44 + CD24 - ( E ) and ALDH1 + ( F ) cells in MCF-7 cells cultured alone (UT) or co-cultured with NBFs underwent indicated treatment. G – I The apoptosis after cisplatin treatment ( G ), the ALDH1 + ( H ) and the CD44 + CD24 - ( I ) proportion of MCF-7 cells cultured alone or co-cultured with untreated or CCL18-treated NBFs transduced with GFP shRNA or IL-6 and IL-8 shRNA ( n = 3). Data expressed as mean ± SEM, *** P < 0.001 compared with NBFs co-cultured with untreated TAMs ( A ), untreated NBFs ( B , D – F ) or CCL18-treated NBFs without shRNA transduction ( G – I ) by two-tailed one-way ANOVA with Dunnett’s multiple comparison test.

    Techniques Used: Inhibition, Cell Culture, Western Blot, Transduction, shRNA, Two Tailed Test

    A Representative western blotting for α-SMA, FAP, CD10 and GPR77 in untreated (UT) or CCL18-treated NBFs transduced with shRNA against GFP or PITPNM3 ( n = 3). B Representative images(up) and diameters(down) of collagen gel contraction assay for NBFs with indicated treatment ( n = 3). C Representative western blotting for total expression and phosphorylation of IKK, IκB and SMAD2/3 in NBFs with indicated treatment ( n = 3). D (left)Representative images of p65 immunofluorescent staining and (right) quantification of p65 nuclear translocation in NBFs with indicated treatment ( n = 3). Scale bars (white line), 50 μm; Scale bars (yellow line), 5 μm. E Localizations of p65 to the promoters of CD10 and GPR77 genes in indicated fibroblasts were analyzed by ChIP assay using anti-p65 Ab or control IgG. F , G QRT–PCR ( F ) and representative western blotting ( G ) for CD10 and GPR77 expression in untreated (UT) or CCL18-activated NBFs treated with DMSO, JSH-23 or BAY117082 ( n = 3). H , I ELISA for IL-8 ( H ) and IL-6 ( I ) levels in the conditioned medium of untreated, CCL18 or TGF-β treated NBFs in the presence of JSH-23, BAY117082 or transduced with GFP or p65 shRNAs ( n = 3). JSH-23, an NF-κB inhibitor. BAY117082, an IKK inhibitor. Data expressed as mean ± SEM, *** P < 0.001 compared with NBFs co-cultured with untreated CCL18-activated NBFs ( B , F , H , I ) or TGF-β treated NBFs ( E ) by two-tailed one-way ANOVA with Dunnett’s multiple comparison test.
    Figure Legend Snippet: A Representative western blotting for α-SMA, FAP, CD10 and GPR77 in untreated (UT) or CCL18-treated NBFs transduced with shRNA against GFP or PITPNM3 ( n = 3). B Representative images(up) and diameters(down) of collagen gel contraction assay for NBFs with indicated treatment ( n = 3). C Representative western blotting for total expression and phosphorylation of IKK, IκB and SMAD2/3 in NBFs with indicated treatment ( n = 3). D (left)Representative images of p65 immunofluorescent staining and (right) quantification of p65 nuclear translocation in NBFs with indicated treatment ( n = 3). Scale bars (white line), 50 μm; Scale bars (yellow line), 5 μm. E Localizations of p65 to the promoters of CD10 and GPR77 genes in indicated fibroblasts were analyzed by ChIP assay using anti-p65 Ab or control IgG. F , G QRT–PCR ( F ) and representative western blotting ( G ) for CD10 and GPR77 expression in untreated (UT) or CCL18-activated NBFs treated with DMSO, JSH-23 or BAY117082 ( n = 3). H , I ELISA for IL-8 ( H ) and IL-6 ( I ) levels in the conditioned medium of untreated, CCL18 or TGF-β treated NBFs in the presence of JSH-23, BAY117082 or transduced with GFP or p65 shRNAs ( n = 3). JSH-23, an NF-κB inhibitor. BAY117082, an IKK inhibitor. Data expressed as mean ± SEM, *** P < 0.001 compared with NBFs co-cultured with untreated CCL18-activated NBFs ( B , F , H , I ) or TGF-β treated NBFs ( E ) by two-tailed one-way ANOVA with Dunnett’s multiple comparison test.

    Techniques Used: Western Blot, Transduction, shRNA, Collagen Gel Contraction Assay, Expressing, Staining, Translocation Assay, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Cell Culture, Two Tailed Test

    A MCF-7 cells were implanted alone or co-injected with NBFs into the mammary fat pads of NOD/SCID mice, and recombinant CCL18 was administrated twice a week and the tumor formation were monitored for up to three months. Xenograft formation rates were shown ( n = 12 per group). Green part represented the proportion of mice fail to develop tumors and red part represented the proportion of mice that developed tumors successfully. * P < 0.05, ** P < 0.01 by Fisher’s exact test. B Quantification for CD10 + GPR77 + fibroblasts(black) and ALDH1 + tumor cells(red) by immunofluorescent staining in the harvested tumors in A ( n = 5 per group). C Quantification for the density of IL6 + fibroblasts(black) and IL8 + fibroblasts(red) determined by immunofluorescent staining in the harvested tumors in A ( n = 5 per group). D , E MCF-7 cells were implanted alone or co-injected with NBFs and docetaxel was administrated one week after implantation concomitantly with or without recombinant CCL18. D Tumor growth was monitored for 7 weeks (mean ± SEM, n = 8 per group). E Representative images for TUNEL + cells in the xenografts related to D (mean ± SEM, n = 8 per group). Scale bars, 25 μm. F-H , MCF-7 cells were implanted without or with NBFs and TAMs into the mammary fat pads of NOD/SCID mice and neutralizing antibody against CCL18 was used to block CCL18 signaling. Docetaxel was administrated 1 week after implantation. F Tumor growth was monitored for 7 weeks (mean ± SEM, n = 8 per group). G Quantification ( n = 5 per group) and ( H ) representative immunofluorescent images for CD163 + CCL18 + macrophages, CD10 + GPR77 + fibroblasts and TUNEL + EPCAM + tumor cells in the harvested tumors in F . Scale bars in H 50 μm. Data expressed as Mean ± SEM, *** P < 0.001 compared with xenografts formed by untreated MCF-7( A , D , E ), xenografts formed by MCF-7 cells co-implanted with NBFs without CCL18 treatment ( B , C ) or xenografts formed by MCF-7 cells co-implanted with NBFs and TAMs without CCL18 neutralizing antibody treatment ( F , G ) by two-tailed one-way ANOVA with Dunnett’s multiple comparison test.
    Figure Legend Snippet: A MCF-7 cells were implanted alone or co-injected with NBFs into the mammary fat pads of NOD/SCID mice, and recombinant CCL18 was administrated twice a week and the tumor formation were monitored for up to three months. Xenograft formation rates were shown ( n = 12 per group). Green part represented the proportion of mice fail to develop tumors and red part represented the proportion of mice that developed tumors successfully. * P < 0.05, ** P < 0.01 by Fisher’s exact test. B Quantification for CD10 + GPR77 + fibroblasts(black) and ALDH1 + tumor cells(red) by immunofluorescent staining in the harvested tumors in A ( n = 5 per group). C Quantification for the density of IL6 + fibroblasts(black) and IL8 + fibroblasts(red) determined by immunofluorescent staining in the harvested tumors in A ( n = 5 per group). D , E MCF-7 cells were implanted alone or co-injected with NBFs and docetaxel was administrated one week after implantation concomitantly with or without recombinant CCL18. D Tumor growth was monitored for 7 weeks (mean ± SEM, n = 8 per group). E Representative images for TUNEL + cells in the xenografts related to D (mean ± SEM, n = 8 per group). Scale bars, 25 μm. F-H , MCF-7 cells were implanted without or with NBFs and TAMs into the mammary fat pads of NOD/SCID mice and neutralizing antibody against CCL18 was used to block CCL18 signaling. Docetaxel was administrated 1 week after implantation. F Tumor growth was monitored for 7 weeks (mean ± SEM, n = 8 per group). G Quantification ( n = 5 per group) and ( H ) representative immunofluorescent images for CD163 + CCL18 + macrophages, CD10 + GPR77 + fibroblasts and TUNEL + EPCAM + tumor cells in the harvested tumors in F . Scale bars in H 50 μm. Data expressed as Mean ± SEM, *** P < 0.001 compared with xenografts formed by untreated MCF-7( A , D , E ), xenografts formed by MCF-7 cells co-implanted with NBFs without CCL18 treatment ( B , C ) or xenografts formed by MCF-7 cells co-implanted with NBFs and TAMs without CCL18 neutralizing antibody treatment ( F , G ) by two-tailed one-way ANOVA with Dunnett’s multiple comparison test.

    Techniques Used: Injection, Recombinant, Staining, TUNEL Assay, Blocking Assay, Two Tailed Test

    Related Articles

    Staining:

    Article Title: CCL18 signaling from tumor-associated macrophages activates fibroblasts to adopt a chemoresistance-inducing phenotype
    Article Snippet: were pretreated with IgG, TGF-β neutralizing antibody (10 µg/mL, R&D, #MAB1835) or CCL18 neutralizing antibody (10 µg/mL, R&D, #AF394). .. Tumor CM was supplemented with CCL18 neutralizing antibody, IL6 neutralizing antibody (10 µg/mL, BD, #554543) or IL8 neutralizing antibody (10 µg/mL, BD, #554726) prior to the experiments. .. To harvest tumor CM, treatment-naive breast carcinoma samples were cut into fragments of approximately 1 mm 3 and then placed on top of spon

    Western Blot:

    Article Title: CCL18 signaling from tumor-associated macrophages activates fibroblasts to adopt a chemoresistance-inducing phenotype
    Article Snippet: were pretreated with IgG, TGF-β neutralizing antibody (10 µg/mL, R&D, #MAB1835) or CCL18 neutralizing antibody (10 µg/mL, R&D, #AF394). .. Tumor CM was supplemented with CCL18 neutralizing antibody, IL6 neutralizing antibody (10 µg/mL, BD, #554543) or IL8 neutralizing antibody (10 µg/mL, BD, #554726) prior to the experiments. .. To harvest tumor CM, treatment-naive breast carcinoma samples were cut into fragments of approximately 1 mm 3 and then placed on top of spon

    Inhibition:

    Article Title: CCL18 signaling from tumor-associated macrophages activates fibroblasts to adopt a chemoresistance-inducing phenotype
    Article Snippet: were pretreated with IgG, TGF-β neutralizing antibody (10 µg/mL, R&D, #MAB1835) or CCL18 neutralizing antibody (10 µg/mL, R&D, #AF394). .. Tumor CM was supplemented with CCL18 neutralizing antibody, IL6 neutralizing antibody (10 µg/mL, BD, #554543) or IL8 neutralizing antibody (10 µg/mL, BD, #554726) prior to the experiments. .. To harvest tumor CM, treatment-naive breast carcinoma samples were cut into fragments of approximately 1 mm 3 and then placed on top of spon

    Cell Culture:

    Article Title: CCL18 signaling from tumor-associated macrophages activates fibroblasts to adopt a chemoresistance-inducing phenotype
    Article Snippet: were pretreated with IgG, TGF-β neutralizing antibody (10 µg/mL, R&D, #MAB1835) or CCL18 neutralizing antibody (10 µg/mL, R&D, #AF394). .. Tumor CM was supplemented with CCL18 neutralizing antibody, IL6 neutralizing antibody (10 µg/mL, BD, #554543) or IL8 neutralizing antibody (10 µg/mL, BD, #554726) prior to the experiments. .. To harvest tumor CM, treatment-naive breast carcinoma samples were cut into fragments of approximately 1 mm 3 and then placed on top of spon

    Transduction:

    Article Title: CCL18 signaling from tumor-associated macrophages activates fibroblasts to adopt a chemoresistance-inducing phenotype
    Article Snippet: were pretreated with IgG, TGF-β neutralizing antibody (10 µg/mL, R&D, #MAB1835) or CCL18 neutralizing antibody (10 µg/mL, R&D, #AF394). .. Tumor CM was supplemented with CCL18 neutralizing antibody, IL6 neutralizing antibody (10 µg/mL, BD, #554543) or IL8 neutralizing antibody (10 µg/mL, BD, #554726) prior to the experiments. .. To harvest tumor CM, treatment-naive breast carcinoma samples were cut into fragments of approximately 1 mm 3 and then placed on top of spon

    shRNA:

    Article Title: CCL18 signaling from tumor-associated macrophages activates fibroblasts to adopt a chemoresistance-inducing phenotype
    Article Snippet: were pretreated with IgG, TGF-β neutralizing antibody (10 µg/mL, R&D, #MAB1835) or CCL18 neutralizing antibody (10 µg/mL, R&D, #AF394). .. Tumor CM was supplemented with CCL18 neutralizing antibody, IL6 neutralizing antibody (10 µg/mL, BD, #554543) or IL8 neutralizing antibody (10 µg/mL, BD, #554726) prior to the experiments. .. To harvest tumor CM, treatment-naive breast carcinoma samples were cut into fragments of approximately 1 mm 3 and then placed on top of spon

    Two Tailed Test:

    Article Title: CCL18 signaling from tumor-associated macrophages activates fibroblasts to adopt a chemoresistance-inducing phenotype
    Article Snippet: were pretreated with IgG, TGF-β neutralizing antibody (10 µg/mL, R&D, #MAB1835) or CCL18 neutralizing antibody (10 µg/mL, R&D, #AF394). .. Tumor CM was supplemented with CCL18 neutralizing antibody, IL6 neutralizing antibody (10 µg/mL, BD, #554543) or IL8 neutralizing antibody (10 µg/mL, BD, #554726) prior to the experiments. .. To harvest tumor CM, treatment-naive breast carcinoma samples were cut into fragments of approximately 1 mm 3 and then placed on top of spon

    Collagen Gel Contraction Assay:

    Article Title: CCL18 signaling from tumor-associated macrophages activates fibroblasts to adopt a chemoresistance-inducing phenotype
    Article Snippet: were pretreated with IgG, TGF-β neutralizing antibody (10 µg/mL, R&D, #MAB1835) or CCL18 neutralizing antibody (10 µg/mL, R&D, #AF394). .. Tumor CM was supplemented with CCL18 neutralizing antibody, IL6 neutralizing antibody (10 µg/mL, BD, #554543) or IL8 neutralizing antibody (10 µg/mL, BD, #554726) prior to the experiments. .. To harvest tumor CM, treatment-naive breast carcinoma samples were cut into fragments of approximately 1 mm 3 and then placed on top of spon

    Expressing:

    Article Title: CCL18 signaling from tumor-associated macrophages activates fibroblasts to adopt a chemoresistance-inducing phenotype
    Article Snippet: were pretreated with IgG, TGF-β neutralizing antibody (10 µg/mL, R&D, #MAB1835) or CCL18 neutralizing antibody (10 µg/mL, R&D, #AF394). .. Tumor CM was supplemented with CCL18 neutralizing antibody, IL6 neutralizing antibody (10 µg/mL, BD, #554543) or IL8 neutralizing antibody (10 µg/mL, BD, #554726) prior to the experiments. .. To harvest tumor CM, treatment-naive breast carcinoma samples were cut into fragments of approximately 1 mm 3 and then placed on top of spon

    Translocation Assay:

    Article Title: CCL18 signaling from tumor-associated macrophages activates fibroblasts to adopt a chemoresistance-inducing phenotype
    Article Snippet: were pretreated with IgG, TGF-β neutralizing antibody (10 µg/mL, R&D, #MAB1835) or CCL18 neutralizing antibody (10 µg/mL, R&D, #AF394). .. Tumor CM was supplemented with CCL18 neutralizing antibody, IL6 neutralizing antibody (10 µg/mL, BD, #554543) or IL8 neutralizing antibody (10 µg/mL, BD, #554726) prior to the experiments. .. To harvest tumor CM, treatment-naive breast carcinoma samples were cut into fragments of approximately 1 mm 3 and then placed on top of spon

    Quantitative RT-PCR:

    Article Title: CCL18 signaling from tumor-associated macrophages activates fibroblasts to adopt a chemoresistance-inducing phenotype
    Article Snippet: were pretreated with IgG, TGF-β neutralizing antibody (10 µg/mL, R&D, #MAB1835) or CCL18 neutralizing antibody (10 µg/mL, R&D, #AF394). .. Tumor CM was supplemented with CCL18 neutralizing antibody, IL6 neutralizing antibody (10 µg/mL, BD, #554543) or IL8 neutralizing antibody (10 µg/mL, BD, #554726) prior to the experiments. .. To harvest tumor CM, treatment-naive breast carcinoma samples were cut into fragments of approximately 1 mm 3 and then placed on top of spon

    Enzyme-linked Immunosorbent Assay:

    Article Title: CCL18 signaling from tumor-associated macrophages activates fibroblasts to adopt a chemoresistance-inducing phenotype
    Article Snippet: were pretreated with IgG, TGF-β neutralizing antibody (10 µg/mL, R&D, #MAB1835) or CCL18 neutralizing antibody (10 µg/mL, R&D, #AF394). .. Tumor CM was supplemented with CCL18 neutralizing antibody, IL6 neutralizing antibody (10 µg/mL, BD, #554543) or IL8 neutralizing antibody (10 µg/mL, BD, #554726) prior to the experiments. .. To harvest tumor CM, treatment-naive breast carcinoma samples were cut into fragments of approximately 1 mm 3 and then placed on top of spon

    Injection:

    Article Title: CCL18 signaling from tumor-associated macrophages activates fibroblasts to adopt a chemoresistance-inducing phenotype
    Article Snippet: were pretreated with IgG, TGF-β neutralizing antibody (10 µg/mL, R&D, #MAB1835) or CCL18 neutralizing antibody (10 µg/mL, R&D, #AF394). .. Tumor CM was supplemented with CCL18 neutralizing antibody, IL6 neutralizing antibody (10 µg/mL, BD, #554543) or IL8 neutralizing antibody (10 µg/mL, BD, #554726) prior to the experiments. .. To harvest tumor CM, treatment-naive breast carcinoma samples were cut into fragments of approximately 1 mm 3 and then placed on top of spon

    Recombinant:

    Article Title: CCL18 signaling from tumor-associated macrophages activates fibroblasts to adopt a chemoresistance-inducing phenotype
    Article Snippet: were pretreated with IgG, TGF-β neutralizing antibody (10 µg/mL, R&D, #MAB1835) or CCL18 neutralizing antibody (10 µg/mL, R&D, #AF394). .. Tumor CM was supplemented with CCL18 neutralizing antibody, IL6 neutralizing antibody (10 µg/mL, BD, #554543) or IL8 neutralizing antibody (10 µg/mL, BD, #554726) prior to the experiments. .. To harvest tumor CM, treatment-naive breast carcinoma samples were cut into fragments of approximately 1 mm 3 and then placed on top of spon

    TUNEL Assay:

    Article Title: CCL18 signaling from tumor-associated macrophages activates fibroblasts to adopt a chemoresistance-inducing phenotype
    Article Snippet: were pretreated with IgG, TGF-β neutralizing antibody (10 µg/mL, R&D, #MAB1835) or CCL18 neutralizing antibody (10 µg/mL, R&D, #AF394). .. Tumor CM was supplemented with CCL18 neutralizing antibody, IL6 neutralizing antibody (10 µg/mL, BD, #554543) or IL8 neutralizing antibody (10 µg/mL, BD, #554726) prior to the experiments. .. To harvest tumor CM, treatment-naive breast carcinoma samples were cut into fragments of approximately 1 mm 3 and then placed on top of spon

    Blocking Assay:

    Article Title: CCL18 signaling from tumor-associated macrophages activates fibroblasts to adopt a chemoresistance-inducing phenotype
    Article Snippet: were pretreated with IgG, TGF-β neutralizing antibody (10 µg/mL, R&D, #MAB1835) or CCL18 neutralizing antibody (10 µg/mL, R&D, #AF394). .. Tumor CM was supplemented with CCL18 neutralizing antibody, IL6 neutralizing antibody (10 µg/mL, BD, #554543) or IL8 neutralizing antibody (10 µg/mL, BD, #554726) prior to the experiments. .. To harvest tumor CM, treatment-naive breast carcinoma samples were cut into fragments of approximately 1 mm 3 and then placed on top of spon



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    NOX4 promotes macrophage migration and M2 polarization . (A) Cytokine array of the CM of the NSCLC cells and NOX4-overexpressed NSCLC cells. (B) The CM of NOX4-overexpression NSCLC cell were treated with anti-CCL7 (20 μg/ml), <t>anti-IL8</t> (20 μg/ml) or anti-CSF-1 (20 μg/ml). Macrophage migration was detected by migration assay. The data represent three independent experiments. *Compared with control, p < 0.05. #Compared with NOX4-overexpression CM, p < 0.05.
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    NOX4 promotes macrophage migration and M2 polarization . (A) Cytokine array of the CM of the NSCLC cells and NOX4-overexpressed NSCLC cells. (B) The CM of NOX4-overexpression NSCLC cell were treated with anti-CCL7 (20 μg/ml), <t>anti-IL8</t> (20 μg/ml) or anti-CSF-1 (20 μg/ml). Macrophage migration was detected by migration assay. The data represent three independent experiments. *Compared with control, p < 0.05. #Compared with NOX4-overexpression CM, p < 0.05.
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    Image Search Results


    A Representative images of H&E staining and CD10/GPR77 immunofluorescent staining in serial sections of the pre-treatment breast cancer biopsies of chemosensitive ( n = 3) and chemoresistant ( n = 3) patients. B , C Western blotting ( B ) for α-SMA, FAP, CD10, and GPR77 and flow cytometric analysis ( C ) for CD10 and GPR77 in primary normal breast fibroblasts (NBFs) treated with pre-treatment tumor conditional medium (CM). D Cytokine arrays of pre-treatment tumor CM, squares indicate the cytokines with significant changes. E Signal intensity of indicated cytokines in the cytokine arrays and their relative fold change between the chemoresistant ( n = 3) and chemosensitive tumors ( n = 3) F Flow cytometric analysis for CD10 and GPR77 in NBFs treated with chemosensitive or chemoresistant tumor CM added without or with neutralizing antibodies against IL6(αIL6), IL8(αIL8) or CCL18(αCCL18). The patients with complete remission (CR) or partial remission (PR) were classified as chemosensitive, while those with stable disease (SD) or progressive disease (PD) were chemoresistant.

    Journal: Oncogene

    Article Title: CCL18 signaling from tumor-associated macrophages activates fibroblasts to adopt a chemoresistance-inducing phenotype

    doi: 10.1038/s41388-022-02540-2

    Figure Lengend Snippet: A Representative images of H&E staining and CD10/GPR77 immunofluorescent staining in serial sections of the pre-treatment breast cancer biopsies of chemosensitive ( n = 3) and chemoresistant ( n = 3) patients. B , C Western blotting ( B ) for α-SMA, FAP, CD10, and GPR77 and flow cytometric analysis ( C ) for CD10 and GPR77 in primary normal breast fibroblasts (NBFs) treated with pre-treatment tumor conditional medium (CM). D Cytokine arrays of pre-treatment tumor CM, squares indicate the cytokines with significant changes. E Signal intensity of indicated cytokines in the cytokine arrays and their relative fold change between the chemoresistant ( n = 3) and chemosensitive tumors ( n = 3) F Flow cytometric analysis for CD10 and GPR77 in NBFs treated with chemosensitive or chemoresistant tumor CM added without or with neutralizing antibodies against IL6(αIL6), IL8(αIL8) or CCL18(αCCL18). The patients with complete remission (CR) or partial remission (PR) were classified as chemosensitive, while those with stable disease (SD) or progressive disease (PD) were chemoresistant.

    Article Snippet: Tumor CM was supplemented with CCL18 neutralizing antibody, IL6 neutralizing antibody (10 µg/mL, BD, #554543) or IL8 neutralizing antibody (10 µg/mL, BD, #554726) prior to the experiments.

    Techniques: Staining, Western Blot

    A The growth inhibition rate of docetaxel (up) and cisplatin (down) on MCF-7, BT474 or BT549 cultured alone (Ctrl) or co-cultured with NBFs underwent indicated treatment ( n = 3). B The growth inhibition rate of docetaxel on MCF-7 (up) and SK-BR3 (down) cells cultured alone (Ctrl) or co-cultured with NBFs underwent indicated treatment ( n = 3). C , D Representative western blotting ( C ) and quantification ( D ) for cleavage of caspase-3 and PARP in SK-BR3 cells cultured alone (Ctrl) or co-cultured with NBFs underwent indicated treatment and challenged with cisplatin ( n = 3). E , F The percentage of CD44 + CD24 - ( E ) and ALDH1 + ( F ) cells in MCF-7 cells cultured alone (UT) or co-cultured with NBFs underwent indicated treatment. G – I The apoptosis after cisplatin treatment ( G ), the ALDH1 + ( H ) and the CD44 + CD24 - ( I ) proportion of MCF-7 cells cultured alone or co-cultured with untreated or CCL18-treated NBFs transduced with GFP shRNA or IL-6 and IL-8 shRNA ( n = 3). Data expressed as mean ± SEM, *** P < 0.001 compared with NBFs co-cultured with untreated TAMs ( A ), untreated NBFs ( B , D – F ) or CCL18-treated NBFs without shRNA transduction ( G – I ) by two-tailed one-way ANOVA with Dunnett’s multiple comparison test.

    Journal: Oncogene

    Article Title: CCL18 signaling from tumor-associated macrophages activates fibroblasts to adopt a chemoresistance-inducing phenotype

    doi: 10.1038/s41388-022-02540-2

    Figure Lengend Snippet: A The growth inhibition rate of docetaxel (up) and cisplatin (down) on MCF-7, BT474 or BT549 cultured alone (Ctrl) or co-cultured with NBFs underwent indicated treatment ( n = 3). B The growth inhibition rate of docetaxel on MCF-7 (up) and SK-BR3 (down) cells cultured alone (Ctrl) or co-cultured with NBFs underwent indicated treatment ( n = 3). C , D Representative western blotting ( C ) and quantification ( D ) for cleavage of caspase-3 and PARP in SK-BR3 cells cultured alone (Ctrl) or co-cultured with NBFs underwent indicated treatment and challenged with cisplatin ( n = 3). E , F The percentage of CD44 + CD24 - ( E ) and ALDH1 + ( F ) cells in MCF-7 cells cultured alone (UT) or co-cultured with NBFs underwent indicated treatment. G – I The apoptosis after cisplatin treatment ( G ), the ALDH1 + ( H ) and the CD44 + CD24 - ( I ) proportion of MCF-7 cells cultured alone or co-cultured with untreated or CCL18-treated NBFs transduced with GFP shRNA or IL-6 and IL-8 shRNA ( n = 3). Data expressed as mean ± SEM, *** P < 0.001 compared with NBFs co-cultured with untreated TAMs ( A ), untreated NBFs ( B , D – F ) or CCL18-treated NBFs without shRNA transduction ( G – I ) by two-tailed one-way ANOVA with Dunnett’s multiple comparison test.

    Article Snippet: Tumor CM was supplemented with CCL18 neutralizing antibody, IL6 neutralizing antibody (10 µg/mL, BD, #554543) or IL8 neutralizing antibody (10 µg/mL, BD, #554726) prior to the experiments.

    Techniques: Inhibition, Cell Culture, Western Blot, Transduction, shRNA, Two Tailed Test

    A Representative western blotting for α-SMA, FAP, CD10 and GPR77 in untreated (UT) or CCL18-treated NBFs transduced with shRNA against GFP or PITPNM3 ( n = 3). B Representative images(up) and diameters(down) of collagen gel contraction assay for NBFs with indicated treatment ( n = 3). C Representative western blotting for total expression and phosphorylation of IKK, IκB and SMAD2/3 in NBFs with indicated treatment ( n = 3). D (left)Representative images of p65 immunofluorescent staining and (right) quantification of p65 nuclear translocation in NBFs with indicated treatment ( n = 3). Scale bars (white line), 50 μm; Scale bars (yellow line), 5 μm. E Localizations of p65 to the promoters of CD10 and GPR77 genes in indicated fibroblasts were analyzed by ChIP assay using anti-p65 Ab or control IgG. F , G QRT–PCR ( F ) and representative western blotting ( G ) for CD10 and GPR77 expression in untreated (UT) or CCL18-activated NBFs treated with DMSO, JSH-23 or BAY117082 ( n = 3). H , I ELISA for IL-8 ( H ) and IL-6 ( I ) levels in the conditioned medium of untreated, CCL18 or TGF-β treated NBFs in the presence of JSH-23, BAY117082 or transduced with GFP or p65 shRNAs ( n = 3). JSH-23, an NF-κB inhibitor. BAY117082, an IKK inhibitor. Data expressed as mean ± SEM, *** P < 0.001 compared with NBFs co-cultured with untreated CCL18-activated NBFs ( B , F , H , I ) or TGF-β treated NBFs ( E ) by two-tailed one-way ANOVA with Dunnett’s multiple comparison test.

    Journal: Oncogene

    Article Title: CCL18 signaling from tumor-associated macrophages activates fibroblasts to adopt a chemoresistance-inducing phenotype

    doi: 10.1038/s41388-022-02540-2

    Figure Lengend Snippet: A Representative western blotting for α-SMA, FAP, CD10 and GPR77 in untreated (UT) or CCL18-treated NBFs transduced with shRNA against GFP or PITPNM3 ( n = 3). B Representative images(up) and diameters(down) of collagen gel contraction assay for NBFs with indicated treatment ( n = 3). C Representative western blotting for total expression and phosphorylation of IKK, IκB and SMAD2/3 in NBFs with indicated treatment ( n = 3). D (left)Representative images of p65 immunofluorescent staining and (right) quantification of p65 nuclear translocation in NBFs with indicated treatment ( n = 3). Scale bars (white line), 50 μm; Scale bars (yellow line), 5 μm. E Localizations of p65 to the promoters of CD10 and GPR77 genes in indicated fibroblasts were analyzed by ChIP assay using anti-p65 Ab or control IgG. F , G QRT–PCR ( F ) and representative western blotting ( G ) for CD10 and GPR77 expression in untreated (UT) or CCL18-activated NBFs treated with DMSO, JSH-23 or BAY117082 ( n = 3). H , I ELISA for IL-8 ( H ) and IL-6 ( I ) levels in the conditioned medium of untreated, CCL18 or TGF-β treated NBFs in the presence of JSH-23, BAY117082 or transduced with GFP or p65 shRNAs ( n = 3). JSH-23, an NF-κB inhibitor. BAY117082, an IKK inhibitor. Data expressed as mean ± SEM, *** P < 0.001 compared with NBFs co-cultured with untreated CCL18-activated NBFs ( B , F , H , I ) or TGF-β treated NBFs ( E ) by two-tailed one-way ANOVA with Dunnett’s multiple comparison test.

    Article Snippet: Tumor CM was supplemented with CCL18 neutralizing antibody, IL6 neutralizing antibody (10 µg/mL, BD, #554543) or IL8 neutralizing antibody (10 µg/mL, BD, #554726) prior to the experiments.

    Techniques: Western Blot, Transduction, shRNA, Collagen Gel Contraction Assay, Expressing, Staining, Translocation Assay, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Cell Culture, Two Tailed Test

    A MCF-7 cells were implanted alone or co-injected with NBFs into the mammary fat pads of NOD/SCID mice, and recombinant CCL18 was administrated twice a week and the tumor formation were monitored for up to three months. Xenograft formation rates were shown ( n = 12 per group). Green part represented the proportion of mice fail to develop tumors and red part represented the proportion of mice that developed tumors successfully. * P < 0.05, ** P < 0.01 by Fisher’s exact test. B Quantification for CD10 + GPR77 + fibroblasts(black) and ALDH1 + tumor cells(red) by immunofluorescent staining in the harvested tumors in A ( n = 5 per group). C Quantification for the density of IL6 + fibroblasts(black) and IL8 + fibroblasts(red) determined by immunofluorescent staining in the harvested tumors in A ( n = 5 per group). D , E MCF-7 cells were implanted alone or co-injected with NBFs and docetaxel was administrated one week after implantation concomitantly with or without recombinant CCL18. D Tumor growth was monitored for 7 weeks (mean ± SEM, n = 8 per group). E Representative images for TUNEL + cells in the xenografts related to D (mean ± SEM, n = 8 per group). Scale bars, 25 μm. F-H , MCF-7 cells were implanted without or with NBFs and TAMs into the mammary fat pads of NOD/SCID mice and neutralizing antibody against CCL18 was used to block CCL18 signaling. Docetaxel was administrated 1 week after implantation. F Tumor growth was monitored for 7 weeks (mean ± SEM, n = 8 per group). G Quantification ( n = 5 per group) and ( H ) representative immunofluorescent images for CD163 + CCL18 + macrophages, CD10 + GPR77 + fibroblasts and TUNEL + EPCAM + tumor cells in the harvested tumors in F . Scale bars in H 50 μm. Data expressed as Mean ± SEM, *** P < 0.001 compared with xenografts formed by untreated MCF-7( A , D , E ), xenografts formed by MCF-7 cells co-implanted with NBFs without CCL18 treatment ( B , C ) or xenografts formed by MCF-7 cells co-implanted with NBFs and TAMs without CCL18 neutralizing antibody treatment ( F , G ) by two-tailed one-way ANOVA with Dunnett’s multiple comparison test.

    Journal: Oncogene

    Article Title: CCL18 signaling from tumor-associated macrophages activates fibroblasts to adopt a chemoresistance-inducing phenotype

    doi: 10.1038/s41388-022-02540-2

    Figure Lengend Snippet: A MCF-7 cells were implanted alone or co-injected with NBFs into the mammary fat pads of NOD/SCID mice, and recombinant CCL18 was administrated twice a week and the tumor formation were monitored for up to three months. Xenograft formation rates were shown ( n = 12 per group). Green part represented the proportion of mice fail to develop tumors and red part represented the proportion of mice that developed tumors successfully. * P < 0.05, ** P < 0.01 by Fisher’s exact test. B Quantification for CD10 + GPR77 + fibroblasts(black) and ALDH1 + tumor cells(red) by immunofluorescent staining in the harvested tumors in A ( n = 5 per group). C Quantification for the density of IL6 + fibroblasts(black) and IL8 + fibroblasts(red) determined by immunofluorescent staining in the harvested tumors in A ( n = 5 per group). D , E MCF-7 cells were implanted alone or co-injected with NBFs and docetaxel was administrated one week after implantation concomitantly with or without recombinant CCL18. D Tumor growth was monitored for 7 weeks (mean ± SEM, n = 8 per group). E Representative images for TUNEL + cells in the xenografts related to D (mean ± SEM, n = 8 per group). Scale bars, 25 μm. F-H , MCF-7 cells were implanted without or with NBFs and TAMs into the mammary fat pads of NOD/SCID mice and neutralizing antibody against CCL18 was used to block CCL18 signaling. Docetaxel was administrated 1 week after implantation. F Tumor growth was monitored for 7 weeks (mean ± SEM, n = 8 per group). G Quantification ( n = 5 per group) and ( H ) representative immunofluorescent images for CD163 + CCL18 + macrophages, CD10 + GPR77 + fibroblasts and TUNEL + EPCAM + tumor cells in the harvested tumors in F . Scale bars in H 50 μm. Data expressed as Mean ± SEM, *** P < 0.001 compared with xenografts formed by untreated MCF-7( A , D , E ), xenografts formed by MCF-7 cells co-implanted with NBFs without CCL18 treatment ( B , C ) or xenografts formed by MCF-7 cells co-implanted with NBFs and TAMs without CCL18 neutralizing antibody treatment ( F , G ) by two-tailed one-way ANOVA with Dunnett’s multiple comparison test.

    Article Snippet: Tumor CM was supplemented with CCL18 neutralizing antibody, IL6 neutralizing antibody (10 µg/mL, BD, #554543) or IL8 neutralizing antibody (10 µg/mL, BD, #554726) prior to the experiments.

    Techniques: Injection, Recombinant, Staining, TUNEL Assay, Blocking Assay, Two Tailed Test

    Fig. 2 Paracrine IL8 was essential for CAFR-induced oxaliplatin resistance in tumor cells. A Cytokine antibody array of CAFS1-CM or CAFR1-CM. CAFR1-CM with different neutralizing antibodies was used to culture Panc-1 (B) and MIAPaCa-2 (C) cells for 3 days. After 48 h of oxaliplatin exposure, cell viability was measured by CCK8. D Panc-1 and MIAPaCa-2 cells were cultured with different concentrations of human recombinant IL8 for 3 days and subsequently treated with oxaliplatin for 48 h. Cell viability was measured by CCK8. E ELISA analysis of the IL-8 levels in CAFS-CM and CAFR-CM of four different chemosensitive and chemoresistant CAF cell lines. Panc-1 and MIAPaCa-2 cells were cultured with IL8 (100 ng/ml) or CAFR1-CM with an anti-IL8 neutralizing antibody (250 ng/ml) for 3 days. Colony formation assay (F, G) and flow cytometry apoptosis analysis (H, I) were performed to evaluate the chemoresistance of pancreatic cancer cells in each group. The results are presented as the mean ± SD of three technical replicates. *P < 0.05; **P < 0.01; ***P < 0.001; ns no significance.

    Journal: Oncogene

    Article Title: Cancer-associated fibroblast-induced lncRNA UPK1A-AS1 confers platinum resistance in pancreatic cancer via efficient double-strand break repair.

    doi: 10.1038/s41388-022-02253-6

    Figure Lengend Snippet: Fig. 2 Paracrine IL8 was essential for CAFR-induced oxaliplatin resistance in tumor cells. A Cytokine antibody array of CAFS1-CM or CAFR1-CM. CAFR1-CM with different neutralizing antibodies was used to culture Panc-1 (B) and MIAPaCa-2 (C) cells for 3 days. After 48 h of oxaliplatin exposure, cell viability was measured by CCK8. D Panc-1 and MIAPaCa-2 cells were cultured with different concentrations of human recombinant IL8 for 3 days and subsequently treated with oxaliplatin for 48 h. Cell viability was measured by CCK8. E ELISA analysis of the IL-8 levels in CAFS-CM and CAFR-CM of four different chemosensitive and chemoresistant CAF cell lines. Panc-1 and MIAPaCa-2 cells were cultured with IL8 (100 ng/ml) or CAFR1-CM with an anti-IL8 neutralizing antibody (250 ng/ml) for 3 days. Colony formation assay (F, G) and flow cytometry apoptosis analysis (H, I) were performed to evaluate the chemoresistance of pancreatic cancer cells in each group. The results are presented as the mean ± SD of three technical replicates. *P < 0.05; **P < 0.01; ***P < 0.001; ns no significance.

    Article Snippet: An anti-IL8 neutralizing antibody and CAPE (S7414, Selleck, Shanghai, China) was added to each group.

    Techniques: Ab Array, Cell Culture, Recombinant, Enzyme-linked Immunosorbent Assay, Colony Assay, Cytometry

    Fig. 4 CAFR-derived IL8 activated the NF-κB signaling pathway to upregulate UPK1A-AS1. A Top 20 upregulated pathways were plotted based on the enriched gene ratio and p value in Panc-1 cells treated with CAFR1-CM compared to CAFS1-CM. B UPK1A-AS1 expression in Panc- 1 and MiaPaCa-2 cells treated with IL8 (100 ng/ml) alone or IL8 and CAPE (2 μM) together for 3 days. C Western blot analysis of IκBα, p-IκBα, p65, and p-p65 protein expression in Panc-1 and MiaPaCa-2 cells treated with CAFR1-CM or IL8. A neutralizing antibody against IL8 was used to deplete IL8 in CAFR1-CM. D Western blot analysis of p65, and p-p65 protein expression in PDAC tissues from platinum-resistant patients and platinum-sensitive patients. E Luciferase reporter assays of Panc-1 cells transfected with a reporter plasmid containing the UPK1A-AS1 promoter, and treated with IL8 or p65 depletion. F, G A conserved p65-binding motif was predicted by JASPAR and schematic images of the potential p65 motif binding sites in the promoter of UPK1A-AS1 are shown. H ChIP analysis of the p65 occupancy at the promoter of UPK1A- AS1 in Panc-1 cells. I Luciferase reporter assays of Panc-1 cells treated with IL8 and transfected with reporter plasmids containing P1, P2 and P3 deletions in the UPK1A-AS1 promoter. The results are presented as the mean ± SD of three technical replicates. **P < 0.01; ***P < 0.001; ns no significance.

    Journal: Oncogene

    Article Title: Cancer-associated fibroblast-induced lncRNA UPK1A-AS1 confers platinum resistance in pancreatic cancer via efficient double-strand break repair.

    doi: 10.1038/s41388-022-02253-6

    Figure Lengend Snippet: Fig. 4 CAFR-derived IL8 activated the NF-κB signaling pathway to upregulate UPK1A-AS1. A Top 20 upregulated pathways were plotted based on the enriched gene ratio and p value in Panc-1 cells treated with CAFR1-CM compared to CAFS1-CM. B UPK1A-AS1 expression in Panc- 1 and MiaPaCa-2 cells treated with IL8 (100 ng/ml) alone or IL8 and CAPE (2 μM) together for 3 days. C Western blot analysis of IκBα, p-IκBα, p65, and p-p65 protein expression in Panc-1 and MiaPaCa-2 cells treated with CAFR1-CM or IL8. A neutralizing antibody against IL8 was used to deplete IL8 in CAFR1-CM. D Western blot analysis of p65, and p-p65 protein expression in PDAC tissues from platinum-resistant patients and platinum-sensitive patients. E Luciferase reporter assays of Panc-1 cells transfected with a reporter plasmid containing the UPK1A-AS1 promoter, and treated with IL8 or p65 depletion. F, G A conserved p65-binding motif was predicted by JASPAR and schematic images of the potential p65 motif binding sites in the promoter of UPK1A-AS1 are shown. H ChIP analysis of the p65 occupancy at the promoter of UPK1A- AS1 in Panc-1 cells. I Luciferase reporter assays of Panc-1 cells treated with IL8 and transfected with reporter plasmids containing P1, P2 and P3 deletions in the UPK1A-AS1 promoter. The results are presented as the mean ± SD of three technical replicates. **P < 0.01; ***P < 0.001; ns no significance.

    Article Snippet: An anti-IL8 neutralizing antibody and CAPE (S7414, Selleck, Shanghai, China) was added to each group.

    Techniques: Derivative Assay, Expressing, Western Blot, Luciferase, Transfection, Plasmid Preparation, Binding Assay

    Fig. 5 UPK1A-AS1 regulated CAFR-induced oxaliplatin resistance in vivo. A qRT-qPCR analysis of UPK1A-AS1 expression in Panc-1 transfected with shNeg or shUPK1A-AS1 lentivirus. B Once the tumors reached 3 mm in diameter, xenograft subcutaneous model receiving an anti-IL8 neutralizing antibody (20 mg/kg) and oxaliplatin (5 mg/kg) once every 3 days. C Representative images of xenograft subcutaneous model. D The changes of tumor volume were monitored and shown. E Xenograft orthotopic model receiving the same treatment as subcutaneous model 12 days after implantation. F Representative IVIS images and pancreatic tumors in orthotopic xenograft model. G, H Analysis of luminescence intensity in orthotopic xenograft model. The relative luminescence intensity = (Xday27-Xday12)/average (shNegday27-shNegday12). I Analysis of orthotopic tumor volume. The results are presented as the mean ± SD. N = 5/per group, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. ns no significance.

    Journal: Oncogene

    Article Title: Cancer-associated fibroblast-induced lncRNA UPK1A-AS1 confers platinum resistance in pancreatic cancer via efficient double-strand break repair.

    doi: 10.1038/s41388-022-02253-6

    Figure Lengend Snippet: Fig. 5 UPK1A-AS1 regulated CAFR-induced oxaliplatin resistance in vivo. A qRT-qPCR analysis of UPK1A-AS1 expression in Panc-1 transfected with shNeg or shUPK1A-AS1 lentivirus. B Once the tumors reached 3 mm in diameter, xenograft subcutaneous model receiving an anti-IL8 neutralizing antibody (20 mg/kg) and oxaliplatin (5 mg/kg) once every 3 days. C Representative images of xenograft subcutaneous model. D The changes of tumor volume were monitored and shown. E Xenograft orthotopic model receiving the same treatment as subcutaneous model 12 days after implantation. F Representative IVIS images and pancreatic tumors in orthotopic xenograft model. G, H Analysis of luminescence intensity in orthotopic xenograft model. The relative luminescence intensity = (Xday27-Xday12)/average (shNegday27-shNegday12). I Analysis of orthotopic tumor volume. The results are presented as the mean ± SD. N = 5/per group, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. ns no significance.

    Article Snippet: An anti-IL8 neutralizing antibody and CAPE (S7414, Selleck, Shanghai, China) was added to each group.

    Techniques: In Vivo, Expressing, Transfection

    Fig. 8 UPK1A-AS1 overexpression correlates with a poor prognosis in PDAC. A Representative image of ISH of UPK1A-AS1 and IHC for IL8. Scale bars = 200 μm. Quantification of IL8 (B) and UPK1A-AS1 (C) staining in tumors from platinum-sensitive and platinum-resistant patients. The results are presented as the mean ± SD of 21 and 54 biological replicates, respectively. D Correlation between UPK1A-AS1 expression and IL8 protein levels in PDAC tissues. E ELISA analysis of the serum IL-8 levels in platinum-resistant patients and platinum-sensitive patients. The results are presented as the mean ± SD. F Kaplan–Meier survival curves of patients who received platinum-based chemotherapy with high or low UPK1A-AS1 expression. G Kaplan–Meier survival curves of patients who received chemotherapy without platinum with high or low UPK1A-AS1 expression. H Graphical illustration of CAFR derived IL8 mediating UPK1A -AS1 activation in PDAC cells to induce oxaliplatin resistance. **P < 0.01; ***P < 0.001.

    Journal: Oncogene

    Article Title: Cancer-associated fibroblast-induced lncRNA UPK1A-AS1 confers platinum resistance in pancreatic cancer via efficient double-strand break repair.

    doi: 10.1038/s41388-022-02253-6

    Figure Lengend Snippet: Fig. 8 UPK1A-AS1 overexpression correlates with a poor prognosis in PDAC. A Representative image of ISH of UPK1A-AS1 and IHC for IL8. Scale bars = 200 μm. Quantification of IL8 (B) and UPK1A-AS1 (C) staining in tumors from platinum-sensitive and platinum-resistant patients. The results are presented as the mean ± SD of 21 and 54 biological replicates, respectively. D Correlation between UPK1A-AS1 expression and IL8 protein levels in PDAC tissues. E ELISA analysis of the serum IL-8 levels in platinum-resistant patients and platinum-sensitive patients. The results are presented as the mean ± SD. F Kaplan–Meier survival curves of patients who received platinum-based chemotherapy with high or low UPK1A-AS1 expression. G Kaplan–Meier survival curves of patients who received chemotherapy without platinum with high or low UPK1A-AS1 expression. H Graphical illustration of CAFR derived IL8 mediating UPK1A -AS1 activation in PDAC cells to induce oxaliplatin resistance. **P < 0.01; ***P < 0.001.

    Article Snippet: An anti-IL8 neutralizing antibody and CAPE (S7414, Selleck, Shanghai, China) was added to each group.

    Techniques: Over Expression, Staining, Expressing, Enzyme-linked Immunosorbent Assay, Derivative Assay, Activation Assay

    NOX4 promotes macrophage migration and M2 polarization . (A) Cytokine array of the CM of the NSCLC cells and NOX4-overexpressed NSCLC cells. (B) The CM of NOX4-overexpression NSCLC cell were treated with anti-CCL7 (20 μg/ml), anti-IL8 (20 μg/ml) or anti-CSF-1 (20 μg/ml). Macrophage migration was detected by migration assay. The data represent three independent experiments. *Compared with control, p < 0.05. #Compared with NOX4-overexpression CM, p < 0.05.

    Journal: Redox Biology

    Article Title: Tumoral NOX4 recruits M2 tumor-associated macrophages via ROS/PI3K signaling-dependent various cytokine production to promote NSCLC growth

    doi: 10.1016/j.redox.2019.101116

    Figure Lengend Snippet: NOX4 promotes macrophage migration and M2 polarization . (A) Cytokine array of the CM of the NSCLC cells and NOX4-overexpressed NSCLC cells. (B) The CM of NOX4-overexpression NSCLC cell were treated with anti-CCL7 (20 μg/ml), anti-IL8 (20 μg/ml) or anti-CSF-1 (20 μg/ml). Macrophage migration was detected by migration assay. The data represent three independent experiments. *Compared with control, p < 0.05. #Compared with NOX4-overexpression CM, p < 0.05.

    Article Snippet: The mouse EGF neutralizing antibody (#AF2028), the human CCL7 neutralizing antibody (#MAB282), IL8 neutralizing antibody (#MAB208) and CSF-1 neutralizing antibody (#AF216) were R&D Systems.

    Techniques: Migration, Over Expression, Control

    High expression of IL6 and IL8 correlated with resistance to RO4929097 treatment in preclinical models. (A) Expression analysis of 60 cytokines secreted from in vitro cultured RO4929097‐resistant NCI‐H460a cells and RO4929097‐sensitive A549 cells. (B) mRNA (qRT‐PCR) and protein expression (ELISA) of IL6 and IL8 in multiple cell lines used for preclinical efficacy studies. Expression of 18S was used as control for qRT‐PCR. Tumor Growth Inhibition (TGI) by RO4929097 of respective xenograft tumors are indicated on the top.

    Journal: Molecular Oncology

    Article Title: High tumor levels of IL6 and IL8 abrogate preclinical efficacy of the γ‐secretase inhibitor, RO4929097

    doi: 10.1016/j.molonc.2011.01.001

    Figure Lengend Snippet: High expression of IL6 and IL8 correlated with resistance to RO4929097 treatment in preclinical models. (A) Expression analysis of 60 cytokines secreted from in vitro cultured RO4929097‐resistant NCI‐H460a cells and RO4929097‐sensitive A549 cells. (B) mRNA (qRT‐PCR) and protein expression (ELISA) of IL6 and IL8 in multiple cell lines used for preclinical efficacy studies. Expression of 18S was used as control for qRT‐PCR. Tumor Growth Inhibition (TGI) by RO4929097 of respective xenograft tumors are indicated on the top.

    Article Snippet: A neutralizing antibody against IL8 was purchased from R&D Systems.

    Techniques: Expressing, In Vitro, Cell Culture, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Inhibition

    Exogenous overexpression of IL6 and IL8 is able to lead to RO4929097 tumor resistance in preclinical models. (A) FACS characterization of IL6 and IL8 overexpressing A549 cells. (B) Protein expression (ELISA) of IL6 and IL8 in IL6 and IL8 overexpressing A549 cells. (C) Characterization of growth in vitro of IL6 and IL8 overexpressing A549 cells. Equal numbers of cells from each cell line were seeded in 35 mm plates, then serially passed by trypsinization and dilution at the same ratio on the indicated days. Cells were counted during each passage and expressed as a percentage of vector control A549 cells each time. (D) in vivo efficacy following RO4929097 treatment of A549 parental, H460a and IL6 and IL8 overexpressing A549 tumors.

    Journal: Molecular Oncology

    Article Title: High tumor levels of IL6 and IL8 abrogate preclinical efficacy of the γ‐secretase inhibitor, RO4929097

    doi: 10.1016/j.molonc.2011.01.001

    Figure Lengend Snippet: Exogenous overexpression of IL6 and IL8 is able to lead to RO4929097 tumor resistance in preclinical models. (A) FACS characterization of IL6 and IL8 overexpressing A549 cells. (B) Protein expression (ELISA) of IL6 and IL8 in IL6 and IL8 overexpressing A549 cells. (C) Characterization of growth in vitro of IL6 and IL8 overexpressing A549 cells. Equal numbers of cells from each cell line were seeded in 35 mm plates, then serially passed by trypsinization and dilution at the same ratio on the indicated days. Cells were counted during each passage and expressed as a percentage of vector control A549 cells each time. (D) in vivo efficacy following RO4929097 treatment of A549 parental, H460a and IL6 and IL8 overexpressing A549 tumors.

    Article Snippet: A neutralizing antibody against IL8 was purchased from R&D Systems.

    Techniques: Over Expression, Expressing, Enzyme-linked Immunosorbent Assay, In Vitro, Plasmid Preparation, In Vivo

    Reducing expression of IL8 sensitizes RO4929097‐resistant tumors to treatment. (A) mRNA (qRT‐PCR) and protein expression (ELISA) of IL6 and IL8 in engineered IL8 shRNA knockdown H460a cells. Expression of 18S was used as control for qRT‐PCR. (B) in vivo efficacy of RO4929097 treatment of IL8 knockdown H460a tumors.(C) in vivo efficacy studies of RO4929097 treatment of H460a tumors in combination with anti‐IL8 antibodies.

    Journal: Molecular Oncology

    Article Title: High tumor levels of IL6 and IL8 abrogate preclinical efficacy of the γ‐secretase inhibitor, RO4929097

    doi: 10.1016/j.molonc.2011.01.001

    Figure Lengend Snippet: Reducing expression of IL8 sensitizes RO4929097‐resistant tumors to treatment. (A) mRNA (qRT‐PCR) and protein expression (ELISA) of IL6 and IL8 in engineered IL8 shRNA knockdown H460a cells. Expression of 18S was used as control for qRT‐PCR. (B) in vivo efficacy of RO4929097 treatment of IL8 knockdown H460a tumors.(C) in vivo efficacy studies of RO4929097 treatment of H460a tumors in combination with anti‐IL8 antibodies.

    Article Snippet: A neutralizing antibody against IL8 was purchased from R&D Systems.

    Techniques: Expressing, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, shRNA, In Vivo

    U87MG and LOX tumors, expressing high levels of IL6 and IL8, are resistant to RO4929097 treatment. (A) mRNA (qRT‐PCR) and protein expression (ELISA) of IL6 and IL8 in U87MG and LOX cells. (B) Hes1 expression (qRT‐PCR) in U87MG and LOX cells in the absence and presence of RO4929097 for 24 h in vitro. Expression of 18S was used as control for qRT‐PCR. (C) in vivo efficacy studies of RO4929097 treatment of U87MG and LOX tumors.

    Journal: Molecular Oncology

    Article Title: High tumor levels of IL6 and IL8 abrogate preclinical efficacy of the γ‐secretase inhibitor, RO4929097

    doi: 10.1016/j.molonc.2011.01.001

    Figure Lengend Snippet: U87MG and LOX tumors, expressing high levels of IL6 and IL8, are resistant to RO4929097 treatment. (A) mRNA (qRT‐PCR) and protein expression (ELISA) of IL6 and IL8 in U87MG and LOX cells. (B) Hes1 expression (qRT‐PCR) in U87MG and LOX cells in the absence and presence of RO4929097 for 24 h in vitro. Expression of 18S was used as control for qRT‐PCR. (C) in vivo efficacy studies of RO4929097 treatment of U87MG and LOX tumors.

    Article Snippet: A neutralizing antibody against IL8 was purchased from R&D Systems.

    Techniques: Expressing, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, In Vitro, In Vivo

    IL6 and IL8 are able to offset the anti‐angiogenic effect of RO4929097 in preclinical models. (A) Selected mouse markers for mRNA expression analysis in xenografted human tumors. (B) mRNA expression analysis (qRT‐PCR) of selected mouse markers in xenografted human tumors. Control for qRT‐PCR of each marker is indicated in the figure. All groups have five tumors with the exception of the control‐treated A549 parental group which has 4 tumors. For all A549‐derived tumors, the average expression in A549 parental tumors was preset to one, then the expression in individual tumors was normalized accordingly. The same normalization approach was applied to H460a‐derived tumors. Statistics: student's t‐test. (C) Hes1 expression (qRT‐PCR) in vector control A549 and IL6 and IL8 overexpressing A549 cells in the absence and presence of RO4929097 for 24 h in vitro. Expression of 18S was used as control for qRT‐PCR.

    Journal: Molecular Oncology

    Article Title: High tumor levels of IL6 and IL8 abrogate preclinical efficacy of the γ‐secretase inhibitor, RO4929097

    doi: 10.1016/j.molonc.2011.01.001

    Figure Lengend Snippet: IL6 and IL8 are able to offset the anti‐angiogenic effect of RO4929097 in preclinical models. (A) Selected mouse markers for mRNA expression analysis in xenografted human tumors. (B) mRNA expression analysis (qRT‐PCR) of selected mouse markers in xenografted human tumors. Control for qRT‐PCR of each marker is indicated in the figure. All groups have five tumors with the exception of the control‐treated A549 parental group which has 4 tumors. For all A549‐derived tumors, the average expression in A549 parental tumors was preset to one, then the expression in individual tumors was normalized accordingly. The same normalization approach was applied to H460a‐derived tumors. Statistics: student's t‐test. (C) Hes1 expression (qRT‐PCR) in vector control A549 and IL6 and IL8 overexpressing A549 cells in the absence and presence of RO4929097 for 24 h in vitro. Expression of 18S was used as control for qRT‐PCR.

    Article Snippet: A neutralizing antibody against IL8 was purchased from R&D Systems.

    Techniques: Expressing, Quantitative RT-PCR, Marker, Derivative Assay, Plasmid Preparation, In Vitro

    Quantitation of pre‐dose IL6 and IL8 plasma levels in patients treated with RO4929097 during Phase I dose escalation. Individual patients are shown in categories of clinical benefit with their corresponding IL6 and IL8 plasma levels. When patient data were treated categorically based on high or low IL8 and IL6 levels, 22.5% of patients (9 out of 40) without clinical benefit have both IL6 and IL8 at high levels (IL6 ≥ 10 pg/ml and IL8 ≥ 40 pg/ml), while only 8.3% of patients (1 out of 12) with clinical benefit have both IL8 and IL6 at high levels. This trend, although positive, is non‐significant given the small patients populations (two‐tailed Fisher's exact test, P = 0.42).

    Journal: Molecular Oncology

    Article Title: High tumor levels of IL6 and IL8 abrogate preclinical efficacy of the γ‐secretase inhibitor, RO4929097

    doi: 10.1016/j.molonc.2011.01.001

    Figure Lengend Snippet: Quantitation of pre‐dose IL6 and IL8 plasma levels in patients treated with RO4929097 during Phase I dose escalation. Individual patients are shown in categories of clinical benefit with their corresponding IL6 and IL8 plasma levels. When patient data were treated categorically based on high or low IL8 and IL6 levels, 22.5% of patients (9 out of 40) without clinical benefit have both IL6 and IL8 at high levels (IL6 ≥ 10 pg/ml and IL8 ≥ 40 pg/ml), while only 8.3% of patients (1 out of 12) with clinical benefit have both IL8 and IL6 at high levels. This trend, although positive, is non‐significant given the small patients populations (two‐tailed Fisher's exact test, P = 0.42).

    Article Snippet: A neutralizing antibody against IL8 was purchased from R&D Systems.

    Techniques: Quantitation Assay, Two Tailed Test