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    Santa Cruz Biotechnology human cxcr1
    A high expression of CXCL8 in human ESCC tissues is associated with the poor prognosis of ESCC patients (A) A double immunofluorescence analysis was performed using anti-CXCL8 (green) and anti-CD11b (red) antibodies on human ESCC tissue. Nuclei were stained with DAPI (blue). Not only CD11b-positive macrophages but also the cancer nest was stained by CXCL8 in human ESCC tissue. Scale bar, 100 μm. (B) Immunohistochemical staining for CXCL8 in human ESCC tissue. Typical images of CXCL8 are shown: negative ( left ), low-intensity ( center ) and high-intensity ( right) compared to the corresponding normal esophageal epithelia. Scale bar, 100 μm. (C) Immunohistochemical staining for <t>CXCR1</t> in human ESCC tissue. Typical images are shown: low-intensity ( left ) and high-intensity ( right ) compared to the corresponding normal esophageal epithelia. Scale bar, 100 μm. (D) Immunohistochemical staining for CXCR2 in human ESCC tissue. Typical images are shown: low-intensity ( left ) and high-intensity ( right ) compared to the corresponding normal esophageal epithelia. Scale bar, 100 μm. (E) Kaplan-Meier analysis of ESCC patients divided into three groups according to their expression of CXCL8: CXCL8-Negative group (n = 14), CXCL8-Low group (n = 43) and CXCL8-High group (n = 13). The log-rank test was performed to determine significance. * p
    Human Cxcr1, supplied by Santa Cruz Biotechnology, 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/result/human cxcr1/product/Santa Cruz Biotechnology
    Average 90 stars, based on 1 article reviews
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    human cxcr1 - by Bioz Stars, 2021-06
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    95
    Addgene inc intron 27
    A high expression of CXCL8 in human ESCC tissues is associated with the poor prognosis of ESCC patients (A) A double immunofluorescence analysis was performed using anti-CXCL8 (green) and anti-CD11b (red) antibodies on human ESCC tissue. Nuclei were stained with DAPI (blue). Not only CD11b-positive macrophages but also the cancer nest was stained by CXCL8 in human ESCC tissue. Scale bar, 100 μm. (B) Immunohistochemical staining for CXCL8 in human ESCC tissue. Typical images of CXCL8 are shown: negative ( left ), low-intensity ( center ) and high-intensity ( right) compared to the corresponding normal esophageal epithelia. Scale bar, 100 μm. (C) Immunohistochemical staining for <t>CXCR1</t> in human ESCC tissue. Typical images are shown: low-intensity ( left ) and high-intensity ( right ) compared to the corresponding normal esophageal epithelia. Scale bar, 100 μm. (D) Immunohistochemical staining for CXCR2 in human ESCC tissue. Typical images are shown: low-intensity ( left ) and high-intensity ( right ) compared to the corresponding normal esophageal epithelia. Scale bar, 100 μm. (E) Kaplan-Meier analysis of ESCC patients divided into three groups according to their expression of CXCL8: CXCL8-Negative group (n = 14), CXCL8-Low group (n = 43) and CXCL8-High group (n = 13). The log-rank test was performed to determine significance. * p
    Intron 27, supplied by Addgene inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/intron 27/product/Addgene inc
    Average 95 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    intron 27 - by Bioz Stars, 2021-06
    95/100 stars
      Buy from Supplier

    Image Search Results


    A high expression of CXCL8 in human ESCC tissues is associated with the poor prognosis of ESCC patients (A) A double immunofluorescence analysis was performed using anti-CXCL8 (green) and anti-CD11b (red) antibodies on human ESCC tissue. Nuclei were stained with DAPI (blue). Not only CD11b-positive macrophages but also the cancer nest was stained by CXCL8 in human ESCC tissue. Scale bar, 100 μm. (B) Immunohistochemical staining for CXCL8 in human ESCC tissue. Typical images of CXCL8 are shown: negative ( left ), low-intensity ( center ) and high-intensity ( right) compared to the corresponding normal esophageal epithelia. Scale bar, 100 μm. (C) Immunohistochemical staining for CXCR1 in human ESCC tissue. Typical images are shown: low-intensity ( left ) and high-intensity ( right ) compared to the corresponding normal esophageal epithelia. Scale bar, 100 μm. (D) Immunohistochemical staining for CXCR2 in human ESCC tissue. Typical images are shown: low-intensity ( left ) and high-intensity ( right ) compared to the corresponding normal esophageal epithelia. Scale bar, 100 μm. (E) Kaplan-Meier analysis of ESCC patients divided into three groups according to their expression of CXCL8: CXCL8-Negative group (n = 14), CXCL8-Low group (n = 43) and CXCL8-High group (n = 13). The log-rank test was performed to determine significance. * p

    Journal: Oncotarget

    Article Title: CXCL8 derived from tumor-associated macrophages and esophageal squamous cell carcinomas contributes to tumor progression by promoting migration and invasion of cancer cells

    doi: 10.18632/oncotarget.22526

    Figure Lengend Snippet: A high expression of CXCL8 in human ESCC tissues is associated with the poor prognosis of ESCC patients (A) A double immunofluorescence analysis was performed using anti-CXCL8 (green) and anti-CD11b (red) antibodies on human ESCC tissue. Nuclei were stained with DAPI (blue). Not only CD11b-positive macrophages but also the cancer nest was stained by CXCL8 in human ESCC tissue. Scale bar, 100 μm. (B) Immunohistochemical staining for CXCL8 in human ESCC tissue. Typical images of CXCL8 are shown: negative ( left ), low-intensity ( center ) and high-intensity ( right) compared to the corresponding normal esophageal epithelia. Scale bar, 100 μm. (C) Immunohistochemical staining for CXCR1 in human ESCC tissue. Typical images are shown: low-intensity ( left ) and high-intensity ( right ) compared to the corresponding normal esophageal epithelia. Scale bar, 100 μm. (D) Immunohistochemical staining for CXCR2 in human ESCC tissue. Typical images are shown: low-intensity ( left ) and high-intensity ( right ) compared to the corresponding normal esophageal epithelia. Scale bar, 100 μm. (E) Kaplan-Meier analysis of ESCC patients divided into three groups according to their expression of CXCL8: CXCL8-Negative group (n = 14), CXCL8-Low group (n = 43) and CXCL8-High group (n = 13). The log-rank test was performed to determine significance. * p

    Article Snippet: CXCR1 and CXCR2 knockdown by small interfering RNA Cancer cell lines were transfected with 20 nM small interfering RNA (siRNA) targeting human CXCR1 (IL-8RA siRNA, sc-40026, Santa Cruz) and CXCR2 (IL-8RB siRNA, sc-40028, Santa Cruz) using Lipofectamine® RNAiMAX (Invitrogen).

    Techniques: Expressing, Immunofluorescence, Staining, Immunohistochemistry

    Akt and Erk1/2 were phosphorylated by CXCL8 through CXCR1 and CXCR2 in the ESCC cell lines (A) The mRNA levels of CXCR1 and CXCR2 in the ESCC cell lines were quantified by RT-PCR. (B) The protein level of CXCR1 and CXCR2 in the ESCC cell lines was confirmed by western blotting. Anti-CXCR1, CXCR2 and β-actin antibodies were used. (C) TE-8, TE-9 and TE-15 cells in serum-free conditions were treated with 10 ng/ml rhCXCL8 for 0, 10, 30 and 60 min. Western blotting was conducted with total protein extracted from ESCC cell lines using specific antibodies against Akt, p-Akt (Ser473), p-Akt (Thr308), Erk1/2, p-Erk1/2 (Thr202/Tyr204) and β-actin. Densitometric analysis of bands was performed with ImageJ (National Institutes of Health, Maryland, USA). The results are mean ± SEM. * p

    Journal: Oncotarget

    Article Title: CXCL8 derived from tumor-associated macrophages and esophageal squamous cell carcinomas contributes to tumor progression by promoting migration and invasion of cancer cells

    doi: 10.18632/oncotarget.22526

    Figure Lengend Snippet: Akt and Erk1/2 were phosphorylated by CXCL8 through CXCR1 and CXCR2 in the ESCC cell lines (A) The mRNA levels of CXCR1 and CXCR2 in the ESCC cell lines were quantified by RT-PCR. (B) The protein level of CXCR1 and CXCR2 in the ESCC cell lines was confirmed by western blotting. Anti-CXCR1, CXCR2 and β-actin antibodies were used. (C) TE-8, TE-9 and TE-15 cells in serum-free conditions were treated with 10 ng/ml rhCXCL8 for 0, 10, 30 and 60 min. Western blotting was conducted with total protein extracted from ESCC cell lines using specific antibodies against Akt, p-Akt (Ser473), p-Akt (Thr308), Erk1/2, p-Erk1/2 (Thr202/Tyr204) and β-actin. Densitometric analysis of bands was performed with ImageJ (National Institutes of Health, Maryland, USA). The results are mean ± SEM. * p

    Article Snippet: CXCR1 and CXCR2 knockdown by small interfering RNA Cancer cell lines were transfected with 20 nM small interfering RNA (siRNA) targeting human CXCR1 (IL-8RA siRNA, sc-40026, Santa Cruz) and CXCR2 (IL-8RB siRNA, sc-40028, Santa Cruz) using Lipofectamine® RNAiMAX (Invitrogen).

    Techniques: Reverse Transcription Polymerase Chain Reaction, Western Blot

    CXCL8 promoted the migration and invasion of the TE-8 cells (A) (i) For the transwell migration assay, TE-8 cells were plated on the transwell in serum-free RPMI-1640 at 5.0 × 10 5 cells/well. rhCXCL8 was added in the upper chamber at 10 ng/ml. The cell inserts were set on 24-well plates in RPMI-1640 with 1% FBS for 24 h. The migrated cells on the underside of the membrane were stained by Diff-Quik and counted. The results are mean ± SEM. Scale bar, 100 μm. (ii) For the transwell invasion assay, TE-8 cells were seeded on a transwell coated with matrigel in serum-free RPMI-1640 at 5.0 × 10 5 cells/well. Recombinant human CXCL8 was added in the transwell at 100 ng/ml. The cell inserts were set on 24-well plates in RPMI-1640 with 1% FBS for 48 h. The invaded cells on the underside of the membrane were stained by Diff-Quik and counted. (B) (i) TE-8 cells were plated on the upper chamber with or without rhCXCL8 at 10 ng/ml combined with the inhibitor against PI3K (LY294002, 10 μM) or MEK1/2 (PD98059, 10 μM). DMSO (0.2 μl/ml) was added to negative control. After 24 h, the migrated cells were counted. (ii) TE-8 cells were plated on the upper transwell coated with matrigel. rhCXCL8 was added in the transwell combined with LY294002 (10 μM) or PD98059 (10 μM). DMSO (0.2 μl/ml) was added to negative control. After 48 h, the invaded cells were counted. (C) TE-8 cells were transfected with 20 nM siRNA targeting CXCR1 and CXCR2 . siNC was transfected to TE-8 as negative control. Effective knockdown of CXCR1 and CXCR2 was confirmed by western blotting using antibodies against CXCR1 and CXCR2. (D) (i) CXCR1 - or CXCR2- silenced TE-8 cells were plated on the upper transwell with rhCXCL8 at 10 ng/ml. After 24 h, the migrated cells were counted. (ii) CXCR1 - or CXCR2 -silenced TE-8 cells were plated on the upper transwell coated with matrigel. rhCXCL8 was added in the transwell at 100 ng/ml. After 48 h, the invaded cells were counted. (E) (i) TE-8 cells were plated on the upper transwell with rhCXCL8 at 10 ng/ml combined with the neutralizing antibody against CXCR1 (0.2 μg/ml) or CXCR2 (1.0 μg/ml). Mouse IgG was added to negative control. The concentrations of neutralizing antibodies were based on the manufacturer's instructions. (ii) TE-8 cells were plated on the upper transwell coated with matrigel. rhCXCL8 was added in the upper transwell at 100 ng/ml combined with the neutralizing antibody against CXCR1 (0.2 μg/ml) or CXCR2 (1.0 μg/ml). Mouse IgG was added to negative control. After 48 h, the invaded cells were counted. NS, not significant; * p

    Journal: Oncotarget

    Article Title: CXCL8 derived from tumor-associated macrophages and esophageal squamous cell carcinomas contributes to tumor progression by promoting migration and invasion of cancer cells

    doi: 10.18632/oncotarget.22526

    Figure Lengend Snippet: CXCL8 promoted the migration and invasion of the TE-8 cells (A) (i) For the transwell migration assay, TE-8 cells were plated on the transwell in serum-free RPMI-1640 at 5.0 × 10 5 cells/well. rhCXCL8 was added in the upper chamber at 10 ng/ml. The cell inserts were set on 24-well plates in RPMI-1640 with 1% FBS for 24 h. The migrated cells on the underside of the membrane were stained by Diff-Quik and counted. The results are mean ± SEM. Scale bar, 100 μm. (ii) For the transwell invasion assay, TE-8 cells were seeded on a transwell coated with matrigel in serum-free RPMI-1640 at 5.0 × 10 5 cells/well. Recombinant human CXCL8 was added in the transwell at 100 ng/ml. The cell inserts were set on 24-well plates in RPMI-1640 with 1% FBS for 48 h. The invaded cells on the underside of the membrane were stained by Diff-Quik and counted. (B) (i) TE-8 cells were plated on the upper chamber with or without rhCXCL8 at 10 ng/ml combined with the inhibitor against PI3K (LY294002, 10 μM) or MEK1/2 (PD98059, 10 μM). DMSO (0.2 μl/ml) was added to negative control. After 24 h, the migrated cells were counted. (ii) TE-8 cells were plated on the upper transwell coated with matrigel. rhCXCL8 was added in the transwell combined with LY294002 (10 μM) or PD98059 (10 μM). DMSO (0.2 μl/ml) was added to negative control. After 48 h, the invaded cells were counted. (C) TE-8 cells were transfected with 20 nM siRNA targeting CXCR1 and CXCR2 . siNC was transfected to TE-8 as negative control. Effective knockdown of CXCR1 and CXCR2 was confirmed by western blotting using antibodies against CXCR1 and CXCR2. (D) (i) CXCR1 - or CXCR2- silenced TE-8 cells were plated on the upper transwell with rhCXCL8 at 10 ng/ml. After 24 h, the migrated cells were counted. (ii) CXCR1 - or CXCR2 -silenced TE-8 cells were plated on the upper transwell coated with matrigel. rhCXCL8 was added in the transwell at 100 ng/ml. After 48 h, the invaded cells were counted. (E) (i) TE-8 cells were plated on the upper transwell with rhCXCL8 at 10 ng/ml combined with the neutralizing antibody against CXCR1 (0.2 μg/ml) or CXCR2 (1.0 μg/ml). Mouse IgG was added to negative control. The concentrations of neutralizing antibodies were based on the manufacturer's instructions. (ii) TE-8 cells were plated on the upper transwell coated with matrigel. rhCXCL8 was added in the upper transwell at 100 ng/ml combined with the neutralizing antibody against CXCR1 (0.2 μg/ml) or CXCR2 (1.0 μg/ml). Mouse IgG was added to negative control. After 48 h, the invaded cells were counted. NS, not significant; * p

    Article Snippet: CXCR1 and CXCR2 knockdown by small interfering RNA Cancer cell lines were transfected with 20 nM small interfering RNA (siRNA) targeting human CXCR1 (IL-8RA siRNA, sc-40026, Santa Cruz) and CXCR2 (IL-8RB siRNA, sc-40028, Santa Cruz) using Lipofectamine® RNAiMAX (Invitrogen).

    Techniques: Migration, Transwell Migration Assay, Staining, Diff-Quik, Transwell Invasion Assay, Recombinant, Negative Control, Transfection, Western Blot

    TAM-like PBMo-derived macrophages induced the migration and invasion of TE-8 cells by activating PI3K and MEK1/2 signals through CXCL8 and CXCR1/2 interaction (A) PBMos (1.0 × 10 5 cells/well) were seeded on the lower chamber of 24-well plates with M-CSF (25 ng/ml) for 6 days to induce PBMo-derived macrophages, then incubated with 50% TE-8 CM to induce TAM-like PBMo-derived macrophages. After 2 days, the media were replaced with serum-free media. (i) TE-8 cells were plated on the upper transwell at 5.0 × 10 5 cells/well and set on the plate. After 24 h, the migrated cells were counted. (ii) TE-8 cells were plated on the upper transwell coated with matrigel at 5.0 × 10 5 cells/well and set on the plate. After 48 h, the invaded cells were counted. Scale bar, 100 μm. (B) (i) TE-8 cells were plated on the upper transwell with the inhibitor against PI3K (LY294002, 10 nM) or MEK1/2 (PD98059, 10 nM). DMSO (0.2 μl/ml) was added to negative control. After 24 h, the migrated cells were counted. (ii) TE-8 cells were plated on the upper matrigel-coated transwell with LY294002 (10 nM) or PD98059 (10 nM). DMSO (0.2 μl/ml) was added to negative control. After 48 h, the invaded cells were counted. (C) (i) TE-8 cells were plated on the upper transwell with the neutralizing antibodies against CXCR1 (0.2 μg/ml), CXCR2 (1.0 μg/ml) or CXCL8 (1.0 μg/ml). Mouse IgG was added to negative control. After 24 h, the migrated cells were counted. The concentrations of neutralizing antibody were based on manufacturer's instructions. (ii) TE-8 cells were plated on the upper matrigel-coated transwell with the neutralizing antibodies against CXCR1 (0.2 μg/ml), CXCR2 (1.0 μg/ml) or CXCL8 (1.0 μg/ml). Mouse IgG was added to negative control. After 48 h, the invaded cells were counted. The results are mean ± SEM. * p

    Journal: Oncotarget

    Article Title: CXCL8 derived from tumor-associated macrophages and esophageal squamous cell carcinomas contributes to tumor progression by promoting migration and invasion of cancer cells

    doi: 10.18632/oncotarget.22526

    Figure Lengend Snippet: TAM-like PBMo-derived macrophages induced the migration and invasion of TE-8 cells by activating PI3K and MEK1/2 signals through CXCL8 and CXCR1/2 interaction (A) PBMos (1.0 × 10 5 cells/well) were seeded on the lower chamber of 24-well plates with M-CSF (25 ng/ml) for 6 days to induce PBMo-derived macrophages, then incubated with 50% TE-8 CM to induce TAM-like PBMo-derived macrophages. After 2 days, the media were replaced with serum-free media. (i) TE-8 cells were plated on the upper transwell at 5.0 × 10 5 cells/well and set on the plate. After 24 h, the migrated cells were counted. (ii) TE-8 cells were plated on the upper transwell coated with matrigel at 5.0 × 10 5 cells/well and set on the plate. After 48 h, the invaded cells were counted. Scale bar, 100 μm. (B) (i) TE-8 cells were plated on the upper transwell with the inhibitor against PI3K (LY294002, 10 nM) or MEK1/2 (PD98059, 10 nM). DMSO (0.2 μl/ml) was added to negative control. After 24 h, the migrated cells were counted. (ii) TE-8 cells were plated on the upper matrigel-coated transwell with LY294002 (10 nM) or PD98059 (10 nM). DMSO (0.2 μl/ml) was added to negative control. After 48 h, the invaded cells were counted. (C) (i) TE-8 cells were plated on the upper transwell with the neutralizing antibodies against CXCR1 (0.2 μg/ml), CXCR2 (1.0 μg/ml) or CXCL8 (1.0 μg/ml). Mouse IgG was added to negative control. After 24 h, the migrated cells were counted. The concentrations of neutralizing antibody were based on manufacturer's instructions. (ii) TE-8 cells were plated on the upper matrigel-coated transwell with the neutralizing antibodies against CXCR1 (0.2 μg/ml), CXCR2 (1.0 μg/ml) or CXCL8 (1.0 μg/ml). Mouse IgG was added to negative control. After 48 h, the invaded cells were counted. The results are mean ± SEM. * p

    Article Snippet: CXCR1 and CXCR2 knockdown by small interfering RNA Cancer cell lines were transfected with 20 nM small interfering RNA (siRNA) targeting human CXCR1 (IL-8RA siRNA, sc-40026, Santa Cruz) and CXCR2 (IL-8RB siRNA, sc-40028, Santa Cruz) using Lipofectamine® RNAiMAX (Invitrogen).

    Techniques: Derivative Assay, Migration, Incubation, Negative Control

    A proposed model of the interaction between ESCC cells and TAMs through CXCL8 in tumor microenvironment Many humoral factors, including IL-4, induced macrophages into TAMs. Then, expression level of CXCL8 was up-regulated in TAMs. CXCL8 secreted from TAMs, as well as from ESCC cells, contributed ESCC cells' migration and invasion by activating Akt and Erk1/2 signals through CXCR1/CXCR2 of ESCC cells.

    Journal: Oncotarget

    Article Title: CXCL8 derived from tumor-associated macrophages and esophageal squamous cell carcinomas contributes to tumor progression by promoting migration and invasion of cancer cells

    doi: 10.18632/oncotarget.22526

    Figure Lengend Snippet: A proposed model of the interaction between ESCC cells and TAMs through CXCL8 in tumor microenvironment Many humoral factors, including IL-4, induced macrophages into TAMs. Then, expression level of CXCL8 was up-regulated in TAMs. CXCL8 secreted from TAMs, as well as from ESCC cells, contributed ESCC cells' migration and invasion by activating Akt and Erk1/2 signals through CXCR1/CXCR2 of ESCC cells.

    Article Snippet: CXCR1 and CXCR2 knockdown by small interfering RNA Cancer cell lines were transfected with 20 nM small interfering RNA (siRNA) targeting human CXCR1 (IL-8RA siRNA, sc-40026, Santa Cruz) and CXCR2 (IL-8RB siRNA, sc-40028, Santa Cruz) using Lipofectamine® RNAiMAX (Invitrogen).

    Techniques: Expressing, Migration