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vector dimethyl sulfoxide dmso  (Selleck Chemicals)


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    Selleck Chemicals vector dimethyl sulfoxide dmso
    STK31 regulates proliferation and the cell cycle in lung cancer cells via the activation of the Wnt/β-catenin <t>pathway.</t> <t>NCIH1299</t> cells were treated with vector + <t>DMSO,</t> vector + 10 µmol/l XAV939 (a Wnt/β-catenin inhibitor), STK31 + DMSO, or STK31 + 10 µmol/l XAV939. (A and B) Cell viability and proliferation were assessed by CCK-8 and BrdU-ELISA assays, respectively, at 0, 24, 48 and 72 h. (C) The proportion of cells in each phase of the cell cycle was evaluated by flow cytometry after 48 h of treatment. (D) Proteins related to β-catenin, c-myc and cyclin D1 protein levels were detected by western blotting. Data are presented as the mean ± SD, **P<0.01 and ***P<0.001 compared to vector, ### P<0.001 compared to STK31. STK31, serine-threonine kinase 31; DMSO, dimethyl sulfoxide; CCK-8, Cell Counting Kit-8; BrdU-ELISA, bromodeoxyuridine-enzyme-linked immunosorbent assay.
    Vector Dimethyl Sulfoxide Dmso, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 97/100, based on 570 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/vector+dimethyl+sulfoxide+dmso/XAV-939/pmc06967196-52-7-23
    Average 97 stars, based on 570 article reviews
    vector dimethyl sulfoxide dmso - by Bioz Stars, 2026-11
    97/100 stars

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    1) Product Images from "STK31 regulates the proliferation and cell cycle of lung cancer cells via the Wnt/β-catenin pathway and feedback regulation by c-myc"

    Article Title: STK31 regulates the proliferation and cell cycle of lung cancer cells via the Wnt/β-catenin pathway and feedback regulation by c-myc

    Journal: Oncology Reports

    doi: 10.3892/or.2019.7441

    STK31 regulates proliferation and the cell cycle in lung cancer cells via the activation of the Wnt/β-catenin pathway. NCIH1299 cells were treated with vector + DMSO, vector + 10 µmol/l XAV939 (a Wnt/β-catenin inhibitor), STK31 + DMSO, or STK31 + 10 µmol/l XAV939. (A and B) Cell viability and proliferation were assessed by CCK-8 and BrdU-ELISA assays, respectively, at 0, 24, 48 and 72 h. (C) The proportion of cells in each phase of the cell cycle was evaluated by flow cytometry after 48 h of treatment. (D) Proteins related to β-catenin, c-myc and cyclin D1 protein levels were detected by western blotting. Data are presented as the mean ± SD, **P<0.01 and ***P<0.001 compared to vector, ### P<0.001 compared to STK31. STK31, serine-threonine kinase 31; DMSO, dimethyl sulfoxide; CCK-8, Cell Counting Kit-8; BrdU-ELISA, bromodeoxyuridine-enzyme-linked immunosorbent assay.
    Figure Legend Snippet: STK31 regulates proliferation and the cell cycle in lung cancer cells via the activation of the Wnt/β-catenin pathway. NCIH1299 cells were treated with vector + DMSO, vector + 10 µmol/l XAV939 (a Wnt/β-catenin inhibitor), STK31 + DMSO, or STK31 + 10 µmol/l XAV939. (A and B) Cell viability and proliferation were assessed by CCK-8 and BrdU-ELISA assays, respectively, at 0, 24, 48 and 72 h. (C) The proportion of cells in each phase of the cell cycle was evaluated by flow cytometry after 48 h of treatment. (D) Proteins related to β-catenin, c-myc and cyclin D1 protein levels were detected by western blotting. Data are presented as the mean ± SD, **P<0.01 and ***P<0.001 compared to vector, ### P<0.001 compared to STK31. STK31, serine-threonine kinase 31; DMSO, dimethyl sulfoxide; CCK-8, Cell Counting Kit-8; BrdU-ELISA, bromodeoxyuridine-enzyme-linked immunosorbent assay.

    Techniques Used: Activation Assay, Plasmid Preparation, CCK-8 Assay, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Western Blot, Cell Counting

    The STK31-mediated regulation of proliferation and the cell cycle in lung cancer cells may act through the positive feedback regulation by c-myc. NCIH358 cells were treated with vector + DMSO, vector + 100 µmol/l 10058-F4 (a c-myc inhibitor), STK31 + DMSO, or STK31 +100 µmol/l 10058-F4. (A and B) Cell viability and proliferation were assessed by CCK-8 and BrdU-ELISA assays, respectively, at 0, 24, 48 and 72 h. (C) The proportion of cells in each phase of the cell cycle was evaluated by flow cytometry after 48 h of treatment. (D) The levels of STK31 mRNA (left) and protein (right) were determined. (E) The expression levels of TRRAP and STK31 were detected by RT-PCR and western blotting. (F) The direct binding of c-myc to the STK31 promoter was confirmed by a ChIP assay. The data are expressed as the mean ± SD, *P<0.05, **P<0.01 and ***P<0.001, compared to vector or shNC, ## P<0.01, ### P<0.001 compared to STK31. STK31, serine-threonine kinase 31; DMSO, dimethyl sulfoxide; CCK-8, Cell Counting Kit-8; TRRAP, transformation/transcription domain-associated protein; ChIP, chromatin immunoprecipitation; BrdU-ELISA, bromodeoxyuridine-enzyme-linked immunosorbent assay.
    Figure Legend Snippet: The STK31-mediated regulation of proliferation and the cell cycle in lung cancer cells may act through the positive feedback regulation by c-myc. NCIH358 cells were treated with vector + DMSO, vector + 100 µmol/l 10058-F4 (a c-myc inhibitor), STK31 + DMSO, or STK31 +100 µmol/l 10058-F4. (A and B) Cell viability and proliferation were assessed by CCK-8 and BrdU-ELISA assays, respectively, at 0, 24, 48 and 72 h. (C) The proportion of cells in each phase of the cell cycle was evaluated by flow cytometry after 48 h of treatment. (D) The levels of STK31 mRNA (left) and protein (right) were determined. (E) The expression levels of TRRAP and STK31 were detected by RT-PCR and western blotting. (F) The direct binding of c-myc to the STK31 promoter was confirmed by a ChIP assay. The data are expressed as the mean ± SD, *P<0.05, **P<0.01 and ***P<0.001, compared to vector or shNC, ## P<0.01, ### P<0.001 compared to STK31. STK31, serine-threonine kinase 31; DMSO, dimethyl sulfoxide; CCK-8, Cell Counting Kit-8; TRRAP, transformation/transcription domain-associated protein; ChIP, chromatin immunoprecipitation; BrdU-ELISA, bromodeoxyuridine-enzyme-linked immunosorbent assay.

    Techniques Used: Plasmid Preparation, CCK-8 Assay, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Expressing, Reverse Transcription Polymerase Chain Reaction, Western Blot, Binding Assay, Cell Counting, Transformation Assay, Chromatin Immunoprecipitation

    Related Articles

    Plasmid Preparation:

    Article Title: STK31 regulates the proliferation and cell cycle of lung cancer cells via the Wnt/β-catenin pathway and feedback regulation by c-myc
    Article Snippet: .. In addition, NCIH1299 cells were treated with vector + dimethyl sulfoxide (DMSO), vector + 10 μmol/l XAV939 (a Wnt/β-catenin inhibitor; cat. no. S1180; Selleck Chemicals, Houston, TX, USA), or STK31 + DMSO, STK31 + 10 μmol/l XAV939, and NCIH358 cells were treated with vector + DMSO, vector + 100 μmol/l 10058-F4 (a c-myc inhibitor; cat. no. S7153; Selleck Chemicals), STK31 + DMSO, or STK31 + 100 μmol/l 10058-F4. ..



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    STK31 regulates proliferation and the cell cycle in lung cancer cells via the activation of the Wnt/β-catenin <t>pathway.</t> <t>NCIH1299</t> cells were treated with vector + <t>DMSO,</t> vector + 10 µmol/l XAV939 (a Wnt/β-catenin inhibitor), STK31 + DMSO, or STK31 + 10 µmol/l XAV939. (A and B) Cell viability and proliferation were assessed by CCK-8 and BrdU-ELISA assays, respectively, at 0, 24, 48 and 72 h. (C) The proportion of cells in each phase of the cell cycle was evaluated by flow cytometry after 48 h of treatment. (D) Proteins related to β-catenin, c-myc and cyclin D1 protein levels were detected by western blotting. Data are presented as the mean ± SD, **P<0.01 and ***P<0.001 compared to vector, ### P<0.001 compared to STK31. STK31, serine-threonine kinase 31; DMSO, dimethyl sulfoxide; CCK-8, Cell Counting Kit-8; BrdU-ELISA, bromodeoxyuridine-enzyme-linked immunosorbent assay.
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    Image Search Results


    STK31 regulates proliferation and the cell cycle in lung cancer cells via the activation of the Wnt/β-catenin pathway. NCIH1299 cells were treated with vector + DMSO, vector + 10 µmol/l XAV939 (a Wnt/β-catenin inhibitor), STK31 + DMSO, or STK31 + 10 µmol/l XAV939. (A and B) Cell viability and proliferation were assessed by CCK-8 and BrdU-ELISA assays, respectively, at 0, 24, 48 and 72 h. (C) The proportion of cells in each phase of the cell cycle was evaluated by flow cytometry after 48 h of treatment. (D) Proteins related to β-catenin, c-myc and cyclin D1 protein levels were detected by western blotting. Data are presented as the mean ± SD, **P<0.01 and ***P<0.001 compared to vector, ### P<0.001 compared to STK31. STK31, serine-threonine kinase 31; DMSO, dimethyl sulfoxide; CCK-8, Cell Counting Kit-8; BrdU-ELISA, bromodeoxyuridine-enzyme-linked immunosorbent assay.

    Journal: Oncology Reports

    Article Title: STK31 regulates the proliferation and cell cycle of lung cancer cells via the Wnt/β-catenin pathway and feedback regulation by c-myc

    doi: 10.3892/or.2019.7441

    Figure Lengend Snippet: STK31 regulates proliferation and the cell cycle in lung cancer cells via the activation of the Wnt/β-catenin pathway. NCIH1299 cells were treated with vector + DMSO, vector + 10 µmol/l XAV939 (a Wnt/β-catenin inhibitor), STK31 + DMSO, or STK31 + 10 µmol/l XAV939. (A and B) Cell viability and proliferation were assessed by CCK-8 and BrdU-ELISA assays, respectively, at 0, 24, 48 and 72 h. (C) The proportion of cells in each phase of the cell cycle was evaluated by flow cytometry after 48 h of treatment. (D) Proteins related to β-catenin, c-myc and cyclin D1 protein levels were detected by western blotting. Data are presented as the mean ± SD, **P<0.01 and ***P<0.001 compared to vector, ### P<0.001 compared to STK31. STK31, serine-threonine kinase 31; DMSO, dimethyl sulfoxide; CCK-8, Cell Counting Kit-8; BrdU-ELISA, bromodeoxyuridine-enzyme-linked immunosorbent assay.

    Article Snippet: In addition, NCIH1299 cells were treated with vector + dimethyl sulfoxide (DMSO), vector + 10 μmol/l XAV939 (a Wnt/β-catenin inhibitor; cat. no. S1180; Selleck Chemicals, Houston, TX, USA), or STK31 + DMSO, STK31 + 10 μmol/l XAV939, and NCIH358 cells were treated with vector + DMSO, vector + 100 μmol/l 10058-F4 (a c-myc inhibitor; cat. no. S7153; Selleck Chemicals), STK31 + DMSO, or STK31 + 100 μmol/l 10058-F4.

    Techniques: Activation Assay, Plasmid Preparation, CCK-8 Assay, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Western Blot, Cell Counting

    The STK31-mediated regulation of proliferation and the cell cycle in lung cancer cells may act through the positive feedback regulation by c-myc. NCIH358 cells were treated with vector + DMSO, vector + 100 µmol/l 10058-F4 (a c-myc inhibitor), STK31 + DMSO, or STK31 +100 µmol/l 10058-F4. (A and B) Cell viability and proliferation were assessed by CCK-8 and BrdU-ELISA assays, respectively, at 0, 24, 48 and 72 h. (C) The proportion of cells in each phase of the cell cycle was evaluated by flow cytometry after 48 h of treatment. (D) The levels of STK31 mRNA (left) and protein (right) were determined. (E) The expression levels of TRRAP and STK31 were detected by RT-PCR and western blotting. (F) The direct binding of c-myc to the STK31 promoter was confirmed by a ChIP assay. The data are expressed as the mean ± SD, *P<0.05, **P<0.01 and ***P<0.001, compared to vector or shNC, ## P<0.01, ### P<0.001 compared to STK31. STK31, serine-threonine kinase 31; DMSO, dimethyl sulfoxide; CCK-8, Cell Counting Kit-8; TRRAP, transformation/transcription domain-associated protein; ChIP, chromatin immunoprecipitation; BrdU-ELISA, bromodeoxyuridine-enzyme-linked immunosorbent assay.

    Journal: Oncology Reports

    Article Title: STK31 regulates the proliferation and cell cycle of lung cancer cells via the Wnt/β-catenin pathway and feedback regulation by c-myc

    doi: 10.3892/or.2019.7441

    Figure Lengend Snippet: The STK31-mediated regulation of proliferation and the cell cycle in lung cancer cells may act through the positive feedback regulation by c-myc. NCIH358 cells were treated with vector + DMSO, vector + 100 µmol/l 10058-F4 (a c-myc inhibitor), STK31 + DMSO, or STK31 +100 µmol/l 10058-F4. (A and B) Cell viability and proliferation were assessed by CCK-8 and BrdU-ELISA assays, respectively, at 0, 24, 48 and 72 h. (C) The proportion of cells in each phase of the cell cycle was evaluated by flow cytometry after 48 h of treatment. (D) The levels of STK31 mRNA (left) and protein (right) were determined. (E) The expression levels of TRRAP and STK31 were detected by RT-PCR and western blotting. (F) The direct binding of c-myc to the STK31 promoter was confirmed by a ChIP assay. The data are expressed as the mean ± SD, *P<0.05, **P<0.01 and ***P<0.001, compared to vector or shNC, ## P<0.01, ### P<0.001 compared to STK31. STK31, serine-threonine kinase 31; DMSO, dimethyl sulfoxide; CCK-8, Cell Counting Kit-8; TRRAP, transformation/transcription domain-associated protein; ChIP, chromatin immunoprecipitation; BrdU-ELISA, bromodeoxyuridine-enzyme-linked immunosorbent assay.

    Article Snippet: In addition, NCIH1299 cells were treated with vector + dimethyl sulfoxide (DMSO), vector + 10 μmol/l XAV939 (a Wnt/β-catenin inhibitor; cat. no. S1180; Selleck Chemicals, Houston, TX, USA), or STK31 + DMSO, STK31 + 10 μmol/l XAV939, and NCIH358 cells were treated with vector + DMSO, vector + 100 μmol/l 10058-F4 (a c-myc inhibitor; cat. no. S7153; Selleck Chemicals), STK31 + DMSO, or STK31 + 100 μmol/l 10058-F4.

    Techniques: Plasmid Preparation, CCK-8 Assay, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Expressing, Reverse Transcription Polymerase Chain Reaction, Western Blot, Binding Assay, Cell Counting, Transformation Assay, Chromatin Immunoprecipitation