5-fluorouracil Search Results


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  • 99
    Millipore fluorouracil 5 fu
    Effects of Shb deletion on disease progression in murine model of CML. (a) Kaplan-Meier curve demonstrating survival of mice receiving either wild type or Shb knockout BCR-ABL transformed bone marrow from <t>5-FU</t> treated mice. (b) Analysis of various disease parameters including liver and spleen weight as well as weight loss at the end-stage of the disease. (c) Bone marrow cell numbers from the tibia, femur and the iliac bones were determined at the time of death. (d and e) Bone marrow cells were stained with fluorescently labeled antibodies directed against Gr-1 and Mac-1 and subsequently analyzed with FACS for GFP ( BCR-ABL ), Mac-1 and GR-1. Plots are representative of a typical experiment. Data are presented as mean ± SEM and based on 15 mice of each genotype from 5 independent experiments (retroviral transformation and transplantation occurring at 5 separate occasions). *denotes p
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    Millipore 5 fu 5 fu
    IL-6 treatment stimulates rRNA transcription by activation of c-myc protein in NCM460 and HepG2 cell lines. ( a ) Real-time–PCR analysis of the 45S rRNA expression in NCM460, HepG2, SW1990 and LS174T cells after 24 h of IL-6 treatment performed with a dose of 50 ng/ml. ( b ) Visualization of rRNA synthesis in control and IL-6-treated NCM460 and HepG2 cells. Cells were labeled with <t>5-FU</t> for 15 min, and 5-FU revealed by specific FITC-conjugated monoclonal antibody. DAPI counterstaining. Scale bar=20 μm. ( c ) Representative western blot and densitometric analysis of c-myc expression in NCM460 and HepG2 cells treated with IL-6 for 1 and 3 h. ( d ) Real-time–PCR analysis of the c-MYC mRNA levels in NCM460 and HepG2 after 1 and 3 h of IL-6 treatment. ( e ) IRES-mediated translation assessed by measuring the FLuc and RLuc activity in control and 4 h IL-6-treated NCM460 and HepG2 cells after 8 h transfection with a bicistronic mRNA transcribed either from pRF (top) or from pR-c-MYC-IRES-F (bottom). ( f ) Time-course analysis of c-myc protein expression in control and 24 h-IL-6-stimulated HepG2 cells, exposed to cycloheximide (CHX) at a concentration of 20 μg/ml. ( g ) Real-time–PCR and western blot analysis of c-MYC expression in scrambled control siRNA (SCR) and in 24 h c-MYC-silenced (MYC−) HepG2 cells exposed to IL-6 for 24 h. The right panel shows the 45S rRNA expression in the same experimental condition. Histograms show the values (mean±s.d.) of three experiments. * P
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    APP Pharmaceuticals 5 fluorouracil 5 fu
    IL-6 treatment stimulates rRNA transcription by activation of c-myc protein in NCM460 and HepG2 cell lines. ( a ) Real-time–PCR analysis of the 45S rRNA expression in NCM460, HepG2, SW1990 and LS174T cells after 24 h of IL-6 treatment performed with a dose of 50 ng/ml. ( b ) Visualization of rRNA synthesis in control and IL-6-treated NCM460 and HepG2 cells. Cells were labeled with <t>5-FU</t> for 15 min, and 5-FU revealed by specific FITC-conjugated monoclonal antibody. DAPI counterstaining. Scale bar=20 μm. ( c ) Representative western blot and densitometric analysis of c-myc expression in NCM460 and HepG2 cells treated with IL-6 for 1 and 3 h. ( d ) Real-time–PCR analysis of the c-MYC mRNA levels in NCM460 and HepG2 after 1 and 3 h of IL-6 treatment. ( e ) IRES-mediated translation assessed by measuring the FLuc and RLuc activity in control and 4 h IL-6-treated NCM460 and HepG2 cells after 8 h transfection with a bicistronic mRNA transcribed either from pRF (top) or from pR-c-MYC-IRES-F (bottom). ( f ) Time-course analysis of c-myc protein expression in control and 24 h-IL-6-stimulated HepG2 cells, exposed to cycloheximide (CHX) at a concentration of 20 μg/ml. ( g ) Real-time–PCR and western blot analysis of c-MYC expression in scrambled control siRNA (SCR) and in 24 h c-MYC-silenced (MYC−) HepG2 cells exposed to IL-6 for 24 h. The right panel shows the 45S rRNA expression in the same experimental condition. Histograms show the values (mean±s.d.) of three experiments. * P
    5 Fluorouracil 5 Fu, supplied by APP Pharmaceuticals, used in various techniques. Bioz Stars score: 90/100, based on 15 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    FUJIFILM 5 fluorouracil 5 fu
    IL-6 treatment stimulates rRNA transcription by activation of c-myc protein in NCM460 and HepG2 cell lines. ( a ) Real-time–PCR analysis of the 45S rRNA expression in NCM460, HepG2, SW1990 and LS174T cells after 24 h of IL-6 treatment performed with a dose of 50 ng/ml. ( b ) Visualization of rRNA synthesis in control and IL-6-treated NCM460 and HepG2 cells. Cells were labeled with <t>5-FU</t> for 15 min, and 5-FU revealed by specific FITC-conjugated monoclonal antibody. DAPI counterstaining. Scale bar=20 μm. ( c ) Representative western blot and densitometric analysis of c-myc expression in NCM460 and HepG2 cells treated with IL-6 for 1 and 3 h. ( d ) Real-time–PCR analysis of the c-MYC mRNA levels in NCM460 and HepG2 after 1 and 3 h of IL-6 treatment. ( e ) IRES-mediated translation assessed by measuring the FLuc and RLuc activity in control and 4 h IL-6-treated NCM460 and HepG2 cells after 8 h transfection with a bicistronic mRNA transcribed either from pRF (top) or from pR-c-MYC-IRES-F (bottom). ( f ) Time-course analysis of c-myc protein expression in control and 24 h-IL-6-stimulated HepG2 cells, exposed to cycloheximide (CHX) at a concentration of 20 μg/ml. ( g ) Real-time–PCR and western blot analysis of c-MYC expression in scrambled control siRNA (SCR) and in 24 h c-MYC-silenced (MYC−) HepG2 cells exposed to IL-6 for 24 h. The right panel shows the 45S rRNA expression in the same experimental condition. Histograms show the values (mean±s.d.) of three experiments. * P
    5 Fluorouracil 5 Fu, supplied by FUJIFILM, used in various techniques. Bioz Stars score: 90/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Merck KGaA 5 fluorouracil 5 fu
    IL-6 treatment stimulates rRNA transcription by activation of c-myc protein in NCM460 and HepG2 cell lines. ( a ) Real-time–PCR analysis of the 45S rRNA expression in NCM460, HepG2, SW1990 and LS174T cells after 24 h of IL-6 treatment performed with a dose of 50 ng/ml. ( b ) Visualization of rRNA synthesis in control and IL-6-treated NCM460 and HepG2 cells. Cells were labeled with <t>5-FU</t> for 15 min, and 5-FU revealed by specific FITC-conjugated monoclonal antibody. DAPI counterstaining. Scale bar=20 μm. ( c ) Representative western blot and densitometric analysis of c-myc expression in NCM460 and HepG2 cells treated with IL-6 for 1 and 3 h. ( d ) Real-time–PCR analysis of the c-MYC mRNA levels in NCM460 and HepG2 after 1 and 3 h of IL-6 treatment. ( e ) IRES-mediated translation assessed by measuring the FLuc and RLuc activity in control and 4 h IL-6-treated NCM460 and HepG2 cells after 8 h transfection with a bicistronic mRNA transcribed either from pRF (top) or from pR-c-MYC-IRES-F (bottom). ( f ) Time-course analysis of c-myc protein expression in control and 24 h-IL-6-stimulated HepG2 cells, exposed to cycloheximide (CHX) at a concentration of 20 μg/ml. ( g ) Real-time–PCR and western blot analysis of c-MYC expression in scrambled control siRNA (SCR) and in 24 h c-MYC-silenced (MYC−) HepG2 cells exposed to IL-6 for 24 h. The right panel shows the 45S rRNA expression in the same experimental condition. Histograms show the values (mean±s.d.) of three experiments. * P
    5 Fluorouracil 5 Fu, supplied by Merck KGaA, used in various techniques. Bioz Stars score: 91/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Nacalai 5 fluorouracil 5 fu
    IL-6 treatment stimulates rRNA transcription by activation of c-myc protein in NCM460 and HepG2 cell lines. ( a ) Real-time–PCR analysis of the 45S rRNA expression in NCM460, HepG2, SW1990 and LS174T cells after 24 h of IL-6 treatment performed with a dose of 50 ng/ml. ( b ) Visualization of rRNA synthesis in control and IL-6-treated NCM460 and HepG2 cells. Cells were labeled with <t>5-FU</t> for 15 min, and 5-FU revealed by specific FITC-conjugated monoclonal antibody. DAPI counterstaining. Scale bar=20 μm. ( c ) Representative western blot and densitometric analysis of c-myc expression in NCM460 and HepG2 cells treated with IL-6 for 1 and 3 h. ( d ) Real-time–PCR analysis of the c-MYC mRNA levels in NCM460 and HepG2 after 1 and 3 h of IL-6 treatment. ( e ) IRES-mediated translation assessed by measuring the FLuc and RLuc activity in control and 4 h IL-6-treated NCM460 and HepG2 cells after 8 h transfection with a bicistronic mRNA transcribed either from pRF (top) or from pR-c-MYC-IRES-F (bottom). ( f ) Time-course analysis of c-myc protein expression in control and 24 h-IL-6-stimulated HepG2 cells, exposed to cycloheximide (CHX) at a concentration of 20 μg/ml. ( g ) Real-time–PCR and western blot analysis of c-MYC expression in scrambled control siRNA (SCR) and in 24 h c-MYC-silenced (MYC−) HepG2 cells exposed to IL-6 for 24 h. The right panel shows the 45S rRNA expression in the same experimental condition. Histograms show the values (mean±s.d.) of three experiments. * P
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    Yabao 5 fluorouracil 5 fu
    IL-6 treatment stimulates rRNA transcription by activation of c-myc protein in NCM460 and HepG2 cell lines. ( a ) Real-time–PCR analysis of the 45S rRNA expression in NCM460, HepG2, SW1990 and LS174T cells after 24 h of IL-6 treatment performed with a dose of 50 ng/ml. ( b ) Visualization of rRNA synthesis in control and IL-6-treated NCM460 and HepG2 cells. Cells were labeled with <t>5-FU</t> for 15 min, and 5-FU revealed by specific FITC-conjugated monoclonal antibody. DAPI counterstaining. Scale bar=20 μm. ( c ) Representative western blot and densitometric analysis of c-myc expression in NCM460 and HepG2 cells treated with IL-6 for 1 and 3 h. ( d ) Real-time–PCR analysis of the c-MYC mRNA levels in NCM460 and HepG2 after 1 and 3 h of IL-6 treatment. ( e ) IRES-mediated translation assessed by measuring the FLuc and RLuc activity in control and 4 h IL-6-treated NCM460 and HepG2 cells after 8 h transfection with a bicistronic mRNA transcribed either from pRF (top) or from pR-c-MYC-IRES-F (bottom). ( f ) Time-course analysis of c-myc protein expression in control and 24 h-IL-6-stimulated HepG2 cells, exposed to cycloheximide (CHX) at a concentration of 20 μg/ml. ( g ) Real-time–PCR and western blot analysis of c-MYC expression in scrambled control siRNA (SCR) and in 24 h c-MYC-silenced (MYC−) HepG2 cells exposed to IL-6 for 24 h. The right panel shows the 45S rRNA expression in the same experimental condition. Histograms show the values (mean±s.d.) of three experiments. * P
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    Shanghai Aladdin Bio-Chem 5 fluorouracil 5 fu
    IL-6 treatment stimulates rRNA transcription by activation of c-myc protein in NCM460 and HepG2 cell lines. ( a ) Real-time–PCR analysis of the 45S rRNA expression in NCM460, HepG2, SW1990 and LS174T cells after 24 h of IL-6 treatment performed with a dose of 50 ng/ml. ( b ) Visualization of rRNA synthesis in control and IL-6-treated NCM460 and HepG2 cells. Cells were labeled with <t>5-FU</t> for 15 min, and 5-FU revealed by specific FITC-conjugated monoclonal antibody. DAPI counterstaining. Scale bar=20 μm. ( c ) Representative western blot and densitometric analysis of c-myc expression in NCM460 and HepG2 cells treated with IL-6 for 1 and 3 h. ( d ) Real-time–PCR analysis of the c-MYC mRNA levels in NCM460 and HepG2 after 1 and 3 h of IL-6 treatment. ( e ) IRES-mediated translation assessed by measuring the FLuc and RLuc activity in control and 4 h IL-6-treated NCM460 and HepG2 cells after 8 h transfection with a bicistronic mRNA transcribed either from pRF (top) or from pR-c-MYC-IRES-F (bottom). ( f ) Time-course analysis of c-myc protein expression in control and 24 h-IL-6-stimulated HepG2 cells, exposed to cycloheximide (CHX) at a concentration of 20 μg/ml. ( g ) Real-time–PCR and western blot analysis of c-MYC expression in scrambled control siRNA (SCR) and in 24 h c-MYC-silenced (MYC−) HepG2 cells exposed to IL-6 for 24 h. The right panel shows the 45S rRNA expression in the same experimental condition. Histograms show the values (mean±s.d.) of three experiments. * P
    5 Fluorouracil 5 Fu, supplied by Shanghai Aladdin Bio-Chem, used in various techniques. Bioz Stars score: 90/100, based on 15 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell migration and invasion assays in wtp53 CRC cells transfected with the combinations shown ( A and B ) p53 knockdown reversed the decrease in cell migration (A) and invasion (B) induced by SRPK2 silencing with <t>5-fluorouracil</t> treatment in HCT116 cells. Original magnification ×200. Data are shown as the mean ± SD. Statistical significance was determined by Student’s t-test; * P
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    Roche 5 fluorouracil 5 fu
    Cell migration and invasion assays in wtp53 CRC cells transfected with the combinations shown ( A and B ) p53 knockdown reversed the decrease in cell migration (A) and invasion (B) induced by SRPK2 silencing with <t>5-fluorouracil</t> treatment in HCT116 cells. Original magnification ×200. Data are shown as the mean ± SD. Statistical significance was determined by Student’s t-test; * P
    5 Fluorouracil 5 Fu, supplied by Roche, used in various techniques. Bioz Stars score: 90/100, based on 28 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Ebewe Pharma 5 fluorouracil 5 fu
    Cell migration and invasion assays in wtp53 CRC cells transfected with the combinations shown ( A and B ) p53 knockdown reversed the decrease in cell migration (A) and invasion (B) induced by SRPK2 silencing with <t>5-fluorouracil</t> treatment in HCT116 cells. Original magnification ×200. Data are shown as the mean ± SD. Statistical significance was determined by Student’s t-test; * P
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    Mayne Pharma 5 fluorouracil 5 fu
    Cell migration and invasion assays in wtp53 CRC cells transfected with the combinations shown ( A and B ) p53 knockdown reversed the decrease in cell migration (A) and invasion (B) induced by SRPK2 silencing with <t>5-fluorouracil</t> treatment in HCT116 cells. Original magnification ×200. Data are shown as the mean ± SD. Statistical significance was determined by Student’s t-test; * P
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    Kyowa Hakko Kirin 5 fluorouracil 5 fu
    Cell migration and invasion assays in wtp53 CRC cells transfected with the combinations shown ( A and B ) p53 knockdown reversed the decrease in cell migration (A) and invasion (B) induced by SRPK2 silencing with <t>5-fluorouracil</t> treatment in HCT116 cells. Original magnification ×200. Data are shown as the mean ± SD. Statistical significance was determined by Student’s t-test; * P
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    Tocris 5 fluorouracil
    ESB increased the chemosensitivity of MKN-45 cells for 24 hours. Cells were co-treated with ESB (40 μg/mL) and a chemotherapeutic agent, such as paclitaxel, <t>5-fluorouracil,</t> cisplatin, etoposide, doxorubicin, or docetaxel at the indicated concentrations and then subjected to MTT assays. Values are expressed as percentages (%) of control, and columns represent means ± SDs. * P
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    InvivoGen 5 fluorouracil 5 fu
    ESB increased the chemosensitivity of MKN-45 cells for 24 hours. Cells were co-treated with ESB (40 μg/mL) and a chemotherapeutic agent, such as paclitaxel, <t>5-fluorouracil,</t> cisplatin, etoposide, doxorubicin, or docetaxel at the indicated concentrations and then subjected to MTT assays. Values are expressed as percentages (%) of control, and columns represent means ± SDs. * P
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    LKT Laboratories 5 fluorouracil
    ESB increased the chemosensitivity of MKN-45 cells for 24 hours. Cells were co-treated with ESB (40 μg/mL) and a chemotherapeutic agent, such as paclitaxel, <t>5-fluorouracil,</t> cisplatin, etoposide, doxorubicin, or docetaxel at the indicated concentrations and then subjected to MTT assays. Values are expressed as percentages (%) of control, and columns represent means ± SDs. * P
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    Image Search Results


    Effects of Shb deletion on disease progression in murine model of CML. (a) Kaplan-Meier curve demonstrating survival of mice receiving either wild type or Shb knockout BCR-ABL transformed bone marrow from 5-FU treated mice. (b) Analysis of various disease parameters including liver and spleen weight as well as weight loss at the end-stage of the disease. (c) Bone marrow cell numbers from the tibia, femur and the iliac bones were determined at the time of death. (d and e) Bone marrow cells were stained with fluorescently labeled antibodies directed against Gr-1 and Mac-1 and subsequently analyzed with FACS for GFP ( BCR-ABL ), Mac-1 and GR-1. Plots are representative of a typical experiment. Data are presented as mean ± SEM and based on 15 mice of each genotype from 5 independent experiments (retroviral transformation and transplantation occurring at 5 separate occasions). *denotes p

    Journal: Journal of Hematology & Oncology

    Article Title: The Src homology-2 protein Shb modulates focal adhesion kinase signaling in a BCR-ABL myeloproliferative disorder causing accelerated progression of disease

    doi: 10.1186/1756-8722-7-45

    Figure Lengend Snippet: Effects of Shb deletion on disease progression in murine model of CML. (a) Kaplan-Meier curve demonstrating survival of mice receiving either wild type or Shb knockout BCR-ABL transformed bone marrow from 5-FU treated mice. (b) Analysis of various disease parameters including liver and spleen weight as well as weight loss at the end-stage of the disease. (c) Bone marrow cell numbers from the tibia, femur and the iliac bones were determined at the time of death. (d and e) Bone marrow cells were stained with fluorescently labeled antibodies directed against Gr-1 and Mac-1 and subsequently analyzed with FACS for GFP ( BCR-ABL ), Mac-1 and GR-1. Plots are representative of a typical experiment. Data are presented as mean ± SEM and based on 15 mice of each genotype from 5 independent experiments (retroviral transformation and transplantation occurring at 5 separate occasions). *denotes p

    Article Snippet: Balb/c Shb wild type or knockout mice 8-10 weeks old were treated with 5 –fluorouracil (5-FU) (Sigma-Aldrich, St. Lois, MO) at a dose of 150 mg/kg body weight 6 days prior to bone marrow isolation, in order to enrich for HSCs.

    Techniques: Mouse Assay, Knock-Out, Transformation Assay, Staining, Labeling, FACS, Transplantation Assay

    Chemotherapeutic drugs induced cell death in ESC1 and Ec109 cells and enriched for a CD44H population of cells. (A) Morphology of ESC1 cells treated with either 12.5 µg/ml DDP (cis-Diammineplatinum(II) dichloride, right upper panel) or 1.25 µg/ml 5-FU (5-Fluorouracil, right lower panel) for 2 days. (B–C) Representative flow cytometry analyses of CD44 expression in ESC1 cells after either DDP (B) or 5-FU (C) treatment. (D) Morphology of Ec109 cells treated with either 50 µg/ml DDP (right upper panel) or 2 µg/ml 5-FU (right lower panel) for 2 days. (E–F) Representative flow cytometry analyses of CD44 expression in Ec109 cells after either DDP (E) or 5-FU (F) treatment. Iso: isotype control; NC: blank control; DMSO: DMSO diluents treated cells; DDP: DDP treated cells; 5-FU: 5-FU treated cells; Scale bar: 50 micrometer.

    Journal: PLoS ONE

    Article Title: Tumor Initiating Cells in Esophageal Squamous Cell Carcinomas Express High Levels of CD44

    doi: 10.1371/journal.pone.0021419

    Figure Lengend Snippet: Chemotherapeutic drugs induced cell death in ESC1 and Ec109 cells and enriched for a CD44H population of cells. (A) Morphology of ESC1 cells treated with either 12.5 µg/ml DDP (cis-Diammineplatinum(II) dichloride, right upper panel) or 1.25 µg/ml 5-FU (5-Fluorouracil, right lower panel) for 2 days. (B–C) Representative flow cytometry analyses of CD44 expression in ESC1 cells after either DDP (B) or 5-FU (C) treatment. (D) Morphology of Ec109 cells treated with either 50 µg/ml DDP (right upper panel) or 2 µg/ml 5-FU (right lower panel) for 2 days. (E–F) Representative flow cytometry analyses of CD44 expression in Ec109 cells after either DDP (E) or 5-FU (F) treatment. Iso: isotype control; NC: blank control; DMSO: DMSO diluents treated cells; DDP: DDP treated cells; 5-FU: 5-FU treated cells; Scale bar: 50 micrometer.

    Article Snippet: All-Trans Retinoic Acid (ATRA), cis-Diammineplatinum(II) dichloride (DPP) and 5-Fluorouracil (5-FU) were from Sigma-Aldrich.

    Techniques: Flow Cytometry, Cytometry, Expressing

    Effect of USP22 on the chemosensitivity of BEL7402 and BEL/FU cells in vitro and in vivo . (A,C) USP22 expression was monitored using western blot analysis in BEL7402 and BEL/FU cells after modulation of USP22. Band intensities were semiquantified using image lab 5.0 software and normalized with AKT or β‐actin. Values are presented as the means under the bands. (B,D) The IC 50 values from the CCK‐8 assay were calculated to assess the sensitivity to 5‐FU, MTX, and ADR. These values are presented as means ± SD from three independent experiments (* P

    Journal: Molecular Oncology

    Article Title: USP22 mediates the multidrug resistance of hepatocellular carcinoma via the SIRT1/AKT/MRP1 signaling pathway

    doi: 10.1002/1878-0261.12067

    Figure Lengend Snippet: Effect of USP22 on the chemosensitivity of BEL7402 and BEL/FU cells in vitro and in vivo . (A,C) USP22 expression was monitored using western blot analysis in BEL7402 and BEL/FU cells after modulation of USP22. Band intensities were semiquantified using image lab 5.0 software and normalized with AKT or β‐actin. Values are presented as the means under the bands. (B,D) The IC 50 values from the CCK‐8 assay were calculated to assess the sensitivity to 5‐FU, MTX, and ADR. These values are presented as means ± SD from three independent experiments (* P

    Article Snippet: 2.2 Reagents and antibodies 5‐Fluorouracil (2,4‐dihydroxy‐5‐fluoropyrimidine), methotrexate (MTX), and ADR (doxorubicin) were purchased from Sigma‐Aldrich (St. Louis, MO, USA).

    Techniques: In Vitro, In Vivo, Expressing, Western Blot, Software, CCK-8 Assay

    Inhibition of the AKT pathway suppresses MRP1 expression and promotes 5‐FU‐induced apoptosis in BEL/FU cells. (A) LY294002 (10 μ m , 20 μ m ) was used to treat BEL/FU cells, and phosphorylated AKT, AKT, phosphorylated GSK‐3β, and MRP1 were monitored using western blot analysis. (B) AKT/MRP1 pathway expression was monitored by western blot analysis in BEL7402 cells with USP22 overexpression and/or LY294002. (C) Cleaved caspase‐3 and cleaved parp were monitored using western blot analysis in cells treated with LY294002 and/or 5‐FU. Band intensities were semiquantified using image lab 5.0 software and normalized with AKT or β‐actin. Values are represented as the means under the bands.

    Journal: Molecular Oncology

    Article Title: USP22 mediates the multidrug resistance of hepatocellular carcinoma via the SIRT1/AKT/MRP1 signaling pathway

    doi: 10.1002/1878-0261.12067

    Figure Lengend Snippet: Inhibition of the AKT pathway suppresses MRP1 expression and promotes 5‐FU‐induced apoptosis in BEL/FU cells. (A) LY294002 (10 μ m , 20 μ m ) was used to treat BEL/FU cells, and phosphorylated AKT, AKT, phosphorylated GSK‐3β, and MRP1 were monitored using western blot analysis. (B) AKT/MRP1 pathway expression was monitored by western blot analysis in BEL7402 cells with USP22 overexpression and/or LY294002. (C) Cleaved caspase‐3 and cleaved parp were monitored using western blot analysis in cells treated with LY294002 and/or 5‐FU. Band intensities were semiquantified using image lab 5.0 software and normalized with AKT or β‐actin. Values are represented as the means under the bands.

    Article Snippet: 2.2 Reagents and antibodies 5‐Fluorouracil (2,4‐dihydroxy‐5‐fluoropyrimidine), methotrexate (MTX), and ADR (doxorubicin) were purchased from Sigma‐Aldrich (St. Louis, MO, USA).

    Techniques: Inhibition, Expressing, Western Blot, Over Expression, Software

    IL-6 treatment stimulates rRNA transcription by activation of c-myc protein in NCM460 and HepG2 cell lines. ( a ) Real-time–PCR analysis of the 45S rRNA expression in NCM460, HepG2, SW1990 and LS174T cells after 24 h of IL-6 treatment performed with a dose of 50 ng/ml. ( b ) Visualization of rRNA synthesis in control and IL-6-treated NCM460 and HepG2 cells. Cells were labeled with 5-FU for 15 min, and 5-FU revealed by specific FITC-conjugated monoclonal antibody. DAPI counterstaining. Scale bar=20 μm. ( c ) Representative western blot and densitometric analysis of c-myc expression in NCM460 and HepG2 cells treated with IL-6 for 1 and 3 h. ( d ) Real-time–PCR analysis of the c-MYC mRNA levels in NCM460 and HepG2 after 1 and 3 h of IL-6 treatment. ( e ) IRES-mediated translation assessed by measuring the FLuc and RLuc activity in control and 4 h IL-6-treated NCM460 and HepG2 cells after 8 h transfection with a bicistronic mRNA transcribed either from pRF (top) or from pR-c-MYC-IRES-F (bottom). ( f ) Time-course analysis of c-myc protein expression in control and 24 h-IL-6-stimulated HepG2 cells, exposed to cycloheximide (CHX) at a concentration of 20 μg/ml. ( g ) Real-time–PCR and western blot analysis of c-MYC expression in scrambled control siRNA (SCR) and in 24 h c-MYC-silenced (MYC−) HepG2 cells exposed to IL-6 for 24 h. The right panel shows the 45S rRNA expression in the same experimental condition. Histograms show the values (mean±s.d.) of three experiments. * P

    Journal: Oncogene

    Article Title: Interleukin 6 downregulates p53 expression and activity by stimulating ribosome biogenesis: a new pathway connecting inflammation to cancer

    doi: 10.1038/onc.2014.1

    Figure Lengend Snippet: IL-6 treatment stimulates rRNA transcription by activation of c-myc protein in NCM460 and HepG2 cell lines. ( a ) Real-time–PCR analysis of the 45S rRNA expression in NCM460, HepG2, SW1990 and LS174T cells after 24 h of IL-6 treatment performed with a dose of 50 ng/ml. ( b ) Visualization of rRNA synthesis in control and IL-6-treated NCM460 and HepG2 cells. Cells were labeled with 5-FU for 15 min, and 5-FU revealed by specific FITC-conjugated monoclonal antibody. DAPI counterstaining. Scale bar=20 μm. ( c ) Representative western blot and densitometric analysis of c-myc expression in NCM460 and HepG2 cells treated with IL-6 for 1 and 3 h. ( d ) Real-time–PCR analysis of the c-MYC mRNA levels in NCM460 and HepG2 after 1 and 3 h of IL-6 treatment. ( e ) IRES-mediated translation assessed by measuring the FLuc and RLuc activity in control and 4 h IL-6-treated NCM460 and HepG2 cells after 8 h transfection with a bicistronic mRNA transcribed either from pRF (top) or from pR-c-MYC-IRES-F (bottom). ( f ) Time-course analysis of c-myc protein expression in control and 24 h-IL-6-stimulated HepG2 cells, exposed to cycloheximide (CHX) at a concentration of 20 μg/ml. ( g ) Real-time–PCR and western blot analysis of c-MYC expression in scrambled control siRNA (SCR) and in 24 h c-MYC-silenced (MYC−) HepG2 cells exposed to IL-6 for 24 h. The right panel shows the 45S rRNA expression in the same experimental condition. Histograms show the values (mean±s.d.) of three experiments. * P

    Article Snippet: Analysis of rRNA synthesis by 5-FU incorporation Cells growing on coverslips were incubated for 15 min in medium containing 2 mM 5-FU (Sigma-Aldrich) and processed as described.

    Techniques: Activation Assay, Real-time Polymerase Chain Reaction, Expressing, Labeling, Western Blot, Activity Assay, Transfection, Concentration Assay

    Cell migration and invasion assays in wtp53 CRC cells transfected with the combinations shown ( A and B ) p53 knockdown reversed the decrease in cell migration (A) and invasion (B) induced by SRPK2 silencing with 5-fluorouracil treatment in HCT116 cells. Original magnification ×200. Data are shown as the mean ± SD. Statistical significance was determined by Student’s t-test; * P

    Journal: Bioscience Reports

    Article Title: Cooperation of SRPK2, Numb and p53 in the malignant biology and chemosensitivity of colorectal cancer

    doi: 10.1042/BSR20191488

    Figure Lengend Snippet: Cell migration and invasion assays in wtp53 CRC cells transfected with the combinations shown ( A and B ) p53 knockdown reversed the decrease in cell migration (A) and invasion (B) induced by SRPK2 silencing with 5-fluorouracil treatment in HCT116 cells. Original magnification ×200. Data are shown as the mean ± SD. Statistical significance was determined by Student’s t-test; * P

    Article Snippet: Briefly, transfected cells were seeded in 96-well plates and treated with a concentration gradient of 5-fluorouracil (Abcam, U.K.) or cisplatin (Abcam, U.K.) for 48 h. Then, each well was incubated with 10 μl CCK-8 (Dojindo, Japan) for 2 h at 37°C.

    Techniques: Migration, Transfection

    Numb and p53 expression in wtp53 CRC cells with the treatment combinations shown under chemical agent treatment ( A and B ) p53 knockdown reversed the up-regulation of wtp53 expression induced by SRPK2 silencing under 5-fluorouracil (A) or cisplatin (B) treatment in HCT116 cells. Data are shown as the mean ± SD. Statistical significance was determined by Student’s t -test; * P

    Journal: Bioscience Reports

    Article Title: Cooperation of SRPK2, Numb and p53 in the malignant biology and chemosensitivity of colorectal cancer

    doi: 10.1042/BSR20191488

    Figure Lengend Snippet: Numb and p53 expression in wtp53 CRC cells with the treatment combinations shown under chemical agent treatment ( A and B ) p53 knockdown reversed the up-regulation of wtp53 expression induced by SRPK2 silencing under 5-fluorouracil (A) or cisplatin (B) treatment in HCT116 cells. Data are shown as the mean ± SD. Statistical significance was determined by Student’s t -test; * P

    Article Snippet: Briefly, transfected cells were seeded in 96-well plates and treated with a concentration gradient of 5-fluorouracil (Abcam, U.K.) or cisplatin (Abcam, U.K.) for 48 h. Then, each well was incubated with 10 μl CCK-8 (Dojindo, Japan) for 2 h at 37°C.

    Techniques: Expressing

    Chemotherapeutic resistance of wtp53 CRC cells treated with chemical agents in the combined protein transfection and expression groups shown ( A and B ) p53 knockdown reversed the decreased chemotherapeutic resistance to 5-fluorouracil (A) or cisplatin (B) induced by SRPK2 silencing in HCT116 cells Data are shown as the mean ± SD. Statistical significance was determined by Student’s t -test. ** P

    Journal: Bioscience Reports

    Article Title: Cooperation of SRPK2, Numb and p53 in the malignant biology and chemosensitivity of colorectal cancer

    doi: 10.1042/BSR20191488

    Figure Lengend Snippet: Chemotherapeutic resistance of wtp53 CRC cells treated with chemical agents in the combined protein transfection and expression groups shown ( A and B ) p53 knockdown reversed the decreased chemotherapeutic resistance to 5-fluorouracil (A) or cisplatin (B) induced by SRPK2 silencing in HCT116 cells Data are shown as the mean ± SD. Statistical significance was determined by Student’s t -test. ** P

    Article Snippet: Briefly, transfected cells were seeded in 96-well plates and treated with a concentration gradient of 5-fluorouracil (Abcam, U.K.) or cisplatin (Abcam, U.K.) for 48 h. Then, each well was incubated with 10 μl CCK-8 (Dojindo, Japan) for 2 h at 37°C.

    Techniques: Transfection, Expressing

    The association of SRPK2 and p53 in mtp53 CRC cell lines ( A and B ) SRPK2 silencing had no effect on p53 protein levels in mtp53 SW480 cells, regardless of treatment with 5-fluorouracil (A) or cisplatin (B). ( C and D ) SRPK2 silencing had no effect on p53 protein levels in mtp53 SW620 cells, regardless of treatment with 5-fluorouracil (C) or cisplatin (D). ( E and F ) SRPK2 overexpression had no effect on p53 protein levels in mtp53 SW480 cells, regardless of treatment with 5-fluorouracil (E) or cisplatin (F). ( G and H ) SRPK2 overexpression had no effect on p53 protein levels in mtp53 SW620 cells, regardless of treatment with 5-fluorouracil (G) or cisplatin (H). Statistical significance was determined by Student’s t -test.

    Journal: Bioscience Reports

    Article Title: Cooperation of SRPK2, Numb and p53 in the malignant biology and chemosensitivity of colorectal cancer

    doi: 10.1042/BSR20191488

    Figure Lengend Snippet: The association of SRPK2 and p53 in mtp53 CRC cell lines ( A and B ) SRPK2 silencing had no effect on p53 protein levels in mtp53 SW480 cells, regardless of treatment with 5-fluorouracil (A) or cisplatin (B). ( C and D ) SRPK2 silencing had no effect on p53 protein levels in mtp53 SW620 cells, regardless of treatment with 5-fluorouracil (C) or cisplatin (D). ( E and F ) SRPK2 overexpression had no effect on p53 protein levels in mtp53 SW480 cells, regardless of treatment with 5-fluorouracil (E) or cisplatin (F). ( G and H ) SRPK2 overexpression had no effect on p53 protein levels in mtp53 SW620 cells, regardless of treatment with 5-fluorouracil (G) or cisplatin (H). Statistical significance was determined by Student’s t -test.

    Article Snippet: Briefly, transfected cells were seeded in 96-well plates and treated with a concentration gradient of 5-fluorouracil (Abcam, U.K.) or cisplatin (Abcam, U.K.) for 48 h. Then, each well was incubated with 10 μl CCK-8 (Dojindo, Japan) for 2 h at 37°C.

    Techniques: Over Expression

    SRPK2 negatively regulates Numb and p53 in wtp53 CRC cells under chemical agent treatment ( A and B ) The association of these 3 proteins in SRPK2-silenced HCT116 cells, with or without 5-fluorouracil (A) or cisplatin (B) treatment. ( C and D ) The association of these three proteins in SRPK2-overexpressing HCT116 cells with or without 5-fluorouracil (C) or cisplatin (D) treatment. Data are shown as the mean ± SD. Statistical significance was determined by Student’s t -test; * P

    Journal: Bioscience Reports

    Article Title: Cooperation of SRPK2, Numb and p53 in the malignant biology and chemosensitivity of colorectal cancer

    doi: 10.1042/BSR20191488

    Figure Lengend Snippet: SRPK2 negatively regulates Numb and p53 in wtp53 CRC cells under chemical agent treatment ( A and B ) The association of these 3 proteins in SRPK2-silenced HCT116 cells, with or without 5-fluorouracil (A) or cisplatin (B) treatment. ( C and D ) The association of these three proteins in SRPK2-overexpressing HCT116 cells with or without 5-fluorouracil (C) or cisplatin (D) treatment. Data are shown as the mean ± SD. Statistical significance was determined by Student’s t -test; * P

    Article Snippet: Briefly, transfected cells were seeded in 96-well plates and treated with a concentration gradient of 5-fluorouracil (Abcam, U.K.) or cisplatin (Abcam, U.K.) for 48 h. Then, each well was incubated with 10 μl CCK-8 (Dojindo, Japan) for 2 h at 37°C.

    Techniques:

    Immunoprecipitation analysis in wtp53 CRC cells without or with 5-fluorouracil treatment ( A–C ) SRPK2 coimmunoprecipitated with Numb and p53 in HCT116 cells without 5-fluorouracil treatment, regardless of whether the SRPK2 (A), Numb (B) or p53 (C) antibody was used. ( D–F ) SRPK2 coimmunoprecipitated with Numb and p53 in HCT116 cells with 5-fluorouracil treatment, regardless of whether the SRPK2 (D), Numb (E) or p53 (F) antibody was used. Input: positive control, IgG: negative control.

    Journal: Bioscience Reports

    Article Title: Cooperation of SRPK2, Numb and p53 in the malignant biology and chemosensitivity of colorectal cancer

    doi: 10.1042/BSR20191488

    Figure Lengend Snippet: Immunoprecipitation analysis in wtp53 CRC cells without or with 5-fluorouracil treatment ( A–C ) SRPK2 coimmunoprecipitated with Numb and p53 in HCT116 cells without 5-fluorouracil treatment, regardless of whether the SRPK2 (A), Numb (B) or p53 (C) antibody was used. ( D–F ) SRPK2 coimmunoprecipitated with Numb and p53 in HCT116 cells with 5-fluorouracil treatment, regardless of whether the SRPK2 (D), Numb (E) or p53 (F) antibody was used. Input: positive control, IgG: negative control.

    Article Snippet: Briefly, transfected cells were seeded in 96-well plates and treated with a concentration gradient of 5-fluorouracil (Abcam, U.K.) or cisplatin (Abcam, U.K.) for 48 h. Then, each well was incubated with 10 μl CCK-8 (Dojindo, Japan) for 2 h at 37°C.

    Techniques: Immunoprecipitation, Positive Control, Negative Control

    SRPK2 regulates the chemotherapeutic resistance of wtp53 CRC cells ( A and B ) SRPK2 silencing significantly decreased the chemotherapeutic resistance to 5-fluorouracil (A) or cisplatin (B) in HCT116 cells. ( C and D ) SRPK2 overexpression significantly enhanced the chemotherapeutic resistance to 5-fluorouracil (C) or cisplatin (D) in HCT116 cells. Data are shown as the mean ± SD. Statistical significance was determined by Student’s t -test. * P

    Journal: Bioscience Reports

    Article Title: Cooperation of SRPK2, Numb and p53 in the malignant biology and chemosensitivity of colorectal cancer

    doi: 10.1042/BSR20191488

    Figure Lengend Snippet: SRPK2 regulates the chemotherapeutic resistance of wtp53 CRC cells ( A and B ) SRPK2 silencing significantly decreased the chemotherapeutic resistance to 5-fluorouracil (A) or cisplatin (B) in HCT116 cells. ( C and D ) SRPK2 overexpression significantly enhanced the chemotherapeutic resistance to 5-fluorouracil (C) or cisplatin (D) in HCT116 cells. Data are shown as the mean ± SD. Statistical significance was determined by Student’s t -test. * P

    Article Snippet: Briefly, transfected cells were seeded in 96-well plates and treated with a concentration gradient of 5-fluorouracil (Abcam, U.K.) or cisplatin (Abcam, U.K.) for 48 h. Then, each well was incubated with 10 μl CCK-8 (Dojindo, Japan) for 2 h at 37°C.

    Techniques: Over Expression

    ESB increased the chemosensitivity of MKN-45 cells for 24 hours. Cells were co-treated with ESB (40 μg/mL) and a chemotherapeutic agent, such as paclitaxel, 5-fluorouracil, cisplatin, etoposide, doxorubicin, or docetaxel at the indicated concentrations and then subjected to MTT assays. Values are expressed as percentages (%) of control, and columns represent means ± SDs. * P

    Journal: Journal of Pharmacopuncture

    Article Title: Inductions of Caspase-, MAPK- and ROS-dependent Apoptosis and Chemotherapeutic Effects Caused by an Ethanol Extract of Scutellaria barbata D. Don in Human Gastric Adenocarcinom Cells

    doi: 10.3831/KPI.2016.19.014

    Figure Lengend Snippet: ESB increased the chemosensitivity of MKN-45 cells for 24 hours. Cells were co-treated with ESB (40 μg/mL) and a chemotherapeutic agent, such as paclitaxel, 5-fluorouracil, cisplatin, etoposide, doxorubicin, or docetaxel at the indicated concentrations and then subjected to MTT assays. Values are expressed as percentages (%) of control, and columns represent means ± SDs. * P

    Article Snippet: The chemotherapeutic agents, namely, paclitaxel, 5-fluorouracil, cisplatin, etoposide, doxorubicin, and docetaxel, were purchased from Tocris Bioscience (Bristol, UK).

    Techniques: MTT Assay