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renal cortical epithelial hrce cell line  (ATCC)


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    ATCC renal cortical epithelial hrce cell line
    Cell viability, cytotoxicity and cell cycle progression in TfRCC cell lines treated with mTOR inhibitors. a , b Cell viability, as measured by MTT assay for TfRCC cell lines and the benign renal <t>epithelial</t> cell line <t>HRCE</t> after 72 h of treatment with up to 1000 nM concentrations of the dual mTORC1/2 inhibitor, AZD8055 ( a ), or selective mTORC1 inhibitor, sirolimus ( b ). Viability in TfRCC cells was suppressed by approximately 80–90% with AZD8055 and 30–50% with sirolimus relative to the untreated (0 nM drug) condition. Both drugs inhibited growth to a greater degree in TfRCC cells than in benign renal cells. c , d Cell cytotoxicity, as measured by LDH release by UOK120 and UOK146 TfRCC cell lines after 48 h of treatment with 1 μM of AZD8055 ( c ) or sirolimus ( d ). Only slight cytotoxicity in UOK120 cells and no cytotoxicity in UOK146 cells was observed after AZD8055 treatment, while sirolimus treatment had no cytotoxic effect. Multi protein inhibitor LY294002 [100 μM] was used as a positive control. e , f Relative fraction of cells in S-phase of the cell cycle, as measured by BrdU incorporation in UOK120 ( e ) and UOK146 ( f ) cell lines treated for 24 h with low (50 nM) and high (500 nM) concentrations of AZD8055 or sirolimus. Dose-dependent reductions in S-phase in both cell lines with either drug mirror the magnitude of reductions observed in cell viability ( a , b ), supporting a predominantly cytostatic mechanism of growth inhibition for both drugs. * p < 0.05; ** p < 0.01; *** p < 0.001; NS = non-significant
    Renal Cortical Epithelial Hrce Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 57 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/renal+cortical+epithelial+hrce+cell+line/Primary+Renal+Cortical+Epithelial+Cells%3B+Normal%2C+Human/pmc06743205-42-16-25
    Average 94 stars, based on 57 article reviews
    renal cortical epithelial hrce cell line - by Bioz Stars, 2026-09
    94/100 stars

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    1) Product Images from "Preclinical efficacy of dual mTORC1/2 inhibitor AZD8055 in renal cell carcinoma harboring a TFE3 gene fusion"

    Article Title: Preclinical efficacy of dual mTORC1/2 inhibitor AZD8055 in renal cell carcinoma harboring a TFE3 gene fusion

    Journal: BMC Cancer

    doi: 10.1186/s12885-019-6096-0

    Cell viability, cytotoxicity and cell cycle progression in TfRCC cell lines treated with mTOR inhibitors. a , b Cell viability, as measured by MTT assay for TfRCC cell lines and the benign renal epithelial cell line HRCE after 72 h of treatment with up to 1000 nM concentrations of the dual mTORC1/2 inhibitor, AZD8055 ( a ), or selective mTORC1 inhibitor, sirolimus ( b ). Viability in TfRCC cells was suppressed by approximately 80–90% with AZD8055 and 30–50% with sirolimus relative to the untreated (0 nM drug) condition. Both drugs inhibited growth to a greater degree in TfRCC cells than in benign renal cells. c , d Cell cytotoxicity, as measured by LDH release by UOK120 and UOK146 TfRCC cell lines after 48 h of treatment with 1 μM of AZD8055 ( c ) or sirolimus ( d ). Only slight cytotoxicity in UOK120 cells and no cytotoxicity in UOK146 cells was observed after AZD8055 treatment, while sirolimus treatment had no cytotoxic effect. Multi protein inhibitor LY294002 [100 μM] was used as a positive control. e , f Relative fraction of cells in S-phase of the cell cycle, as measured by BrdU incorporation in UOK120 ( e ) and UOK146 ( f ) cell lines treated for 24 h with low (50 nM) and high (500 nM) concentrations of AZD8055 or sirolimus. Dose-dependent reductions in S-phase in both cell lines with either drug mirror the magnitude of reductions observed in cell viability ( a , b ), supporting a predominantly cytostatic mechanism of growth inhibition for both drugs. * p < 0.05; ** p < 0.01; *** p < 0.001; NS = non-significant
    Figure Legend Snippet: Cell viability, cytotoxicity and cell cycle progression in TfRCC cell lines treated with mTOR inhibitors. a , b Cell viability, as measured by MTT assay for TfRCC cell lines and the benign renal epithelial cell line HRCE after 72 h of treatment with up to 1000 nM concentrations of the dual mTORC1/2 inhibitor, AZD8055 ( a ), or selective mTORC1 inhibitor, sirolimus ( b ). Viability in TfRCC cells was suppressed by approximately 80–90% with AZD8055 and 30–50% with sirolimus relative to the untreated (0 nM drug) condition. Both drugs inhibited growth to a greater degree in TfRCC cells than in benign renal cells. c , d Cell cytotoxicity, as measured by LDH release by UOK120 and UOK146 TfRCC cell lines after 48 h of treatment with 1 μM of AZD8055 ( c ) or sirolimus ( d ). Only slight cytotoxicity in UOK120 cells and no cytotoxicity in UOK146 cells was observed after AZD8055 treatment, while sirolimus treatment had no cytotoxic effect. Multi protein inhibitor LY294002 [100 μM] was used as a positive control. e , f Relative fraction of cells in S-phase of the cell cycle, as measured by BrdU incorporation in UOK120 ( e ) and UOK146 ( f ) cell lines treated for 24 h with low (50 nM) and high (500 nM) concentrations of AZD8055 or sirolimus. Dose-dependent reductions in S-phase in both cell lines with either drug mirror the magnitude of reductions observed in cell viability ( a , b ), supporting a predominantly cytostatic mechanism of growth inhibition for both drugs. * p < 0.05; ** p < 0.01; *** p < 0.001; NS = non-significant

    Techniques Used: MTT Assay, Positive Control, BrdU Incorporation Assay, Inhibition

    Related Articles

    MTT Assay:

    Article Title: Preclinical efficacy of dual mTORC1/2 inhibitor AZD8055 in renal cell carcinoma harboring a TFE3 gene fusion
    Article Snippet: Collection of this material was approved by the Institutional Review Board of the National Cancer Institute and all patients had provided written informed consent.Collection of this material was approved by the Institutional Review Board of the National Cancer Institute and all patients had provided written informed consent.. RCC4 was obtained from ECACC General Cell Collection (Salisbury, UK; Cat Nr. 03112702) and the human renal cortical epithelial (HRCE) cell line was obtained from ATCC (Manassas, VA; Cat Nr. PCS-400-011).. All cell lines were maintained in vitro in DMEM media supplemented with L-glutamine (4 mM), sodium pyruvate (110 mg/l), glucose (4.5 g/l), and 1X essential amino acids (Gibco, Gaithersburg, MD), with or without 10% fetal bovine serum (Sigma Aldrich, St. Luis, MO).All cell lines were maintained in vitro in DMEM media supplemented with L-glutamine (4 mM), sodium pyruvate (110 mg/l), glucose (4.5 g/l), and 1X essential amino acids (Gibco, Gaithersburg, MD), with or without 10% fetal bovine serum (Sigma Aldrich, St. Luis, MO).

    Positive Control:

    Article Title: Preclinical efficacy of dual mTORC1/2 inhibitor AZD8055 in renal cell carcinoma harboring a TFE3 gene fusion
    Article Snippet: Collection of this material was approved by the Institutional Review Board of the National Cancer Institute and all patients had provided written informed consent.Collection of this material was approved by the Institutional Review Board of the National Cancer Institute and all patients had provided written informed consent.. RCC4 was obtained from ECACC General Cell Collection (Salisbury, UK; Cat Nr. 03112702) and the human renal cortical epithelial (HRCE) cell line was obtained from ATCC (Manassas, VA; Cat Nr. PCS-400-011).. All cell lines were maintained in vitro in DMEM media supplemented with L-glutamine (4 mM), sodium pyruvate (110 mg/l), glucose (4.5 g/l), and 1X essential amino acids (Gibco, Gaithersburg, MD), with or without 10% fetal bovine serum (Sigma Aldrich, St. Luis, MO).All cell lines were maintained in vitro in DMEM media supplemented with L-glutamine (4 mM), sodium pyruvate (110 mg/l), glucose (4.5 g/l), and 1X essential amino acids (Gibco, Gaithersburg, MD), with or without 10% fetal bovine serum (Sigma Aldrich, St. Luis, MO).

    BrdU Incorporation Assay:

    Article Title: Preclinical efficacy of dual mTORC1/2 inhibitor AZD8055 in renal cell carcinoma harboring a TFE3 gene fusion
    Article Snippet: Collection of this material was approved by the Institutional Review Board of the National Cancer Institute and all patients had provided written informed consent.Collection of this material was approved by the Institutional Review Board of the National Cancer Institute and all patients had provided written informed consent.. RCC4 was obtained from ECACC General Cell Collection (Salisbury, UK; Cat Nr. 03112702) and the human renal cortical epithelial (HRCE) cell line was obtained from ATCC (Manassas, VA; Cat Nr. PCS-400-011).. All cell lines were maintained in vitro in DMEM media supplemented with L-glutamine (4 mM), sodium pyruvate (110 mg/l), glucose (4.5 g/l), and 1X essential amino acids (Gibco, Gaithersburg, MD), with or without 10% fetal bovine serum (Sigma Aldrich, St. Luis, MO).All cell lines were maintained in vitro in DMEM media supplemented with L-glutamine (4 mM), sodium pyruvate (110 mg/l), glucose (4.5 g/l), and 1X essential amino acids (Gibco, Gaithersburg, MD), with or without 10% fetal bovine serum (Sigma Aldrich, St. Luis, MO).

    Inhibition:

    Article Title: Preclinical efficacy of dual mTORC1/2 inhibitor AZD8055 in renal cell carcinoma harboring a TFE3 gene fusion
    Article Snippet: Collection of this material was approved by the Institutional Review Board of the National Cancer Institute and all patients had provided written informed consent.Collection of this material was approved by the Institutional Review Board of the National Cancer Institute and all patients had provided written informed consent.. RCC4 was obtained from ECACC General Cell Collection (Salisbury, UK; Cat Nr. 03112702) and the human renal cortical epithelial (HRCE) cell line was obtained from ATCC (Manassas, VA; Cat Nr. PCS-400-011).. All cell lines were maintained in vitro in DMEM media supplemented with L-glutamine (4 mM), sodium pyruvate (110 mg/l), glucose (4.5 g/l), and 1X essential amino acids (Gibco, Gaithersburg, MD), with or without 10% fetal bovine serum (Sigma Aldrich, St. Luis, MO).All cell lines were maintained in vitro in DMEM media supplemented with L-glutamine (4 mM), sodium pyruvate (110 mg/l), glucose (4.5 g/l), and 1X essential amino acids (Gibco, Gaithersburg, MD), with or without 10% fetal bovine serum (Sigma Aldrich, St. Luis, MO).



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    Cell viability, cytotoxicity and cell cycle progression in TfRCC cell lines treated with mTOR inhibitors. a , b Cell viability, as measured by MTT assay for TfRCC cell lines and the benign renal <t>epithelial</t> cell line <t>HRCE</t> after 72 h of treatment with up to 1000 nM concentrations of the dual mTORC1/2 inhibitor, AZD8055 ( a ), or selective mTORC1 inhibitor, sirolimus ( b ). Viability in TfRCC cells was suppressed by approximately 80–90% with AZD8055 and 30–50% with sirolimus relative to the untreated (0 nM drug) condition. Both drugs inhibited growth to a greater degree in TfRCC cells than in benign renal cells. c , d Cell cytotoxicity, as measured by LDH release by UOK120 and UOK146 TfRCC cell lines after 48 h of treatment with 1 μM of AZD8055 ( c ) or sirolimus ( d ). Only slight cytotoxicity in UOK120 cells and no cytotoxicity in UOK146 cells was observed after AZD8055 treatment, while sirolimus treatment had no cytotoxic effect. Multi protein inhibitor LY294002 [100 μM] was used as a positive control. e , f Relative fraction of cells in S-phase of the cell cycle, as measured by BrdU incorporation in UOK120 ( e ) and UOK146 ( f ) cell lines treated for 24 h with low (50 nM) and high (500 nM) concentrations of AZD8055 or sirolimus. Dose-dependent reductions in S-phase in both cell lines with either drug mirror the magnitude of reductions observed in cell viability ( a , b ), supporting a predominantly cytostatic mechanism of growth inhibition for both drugs. * p < 0.05; ** p < 0.01; *** p < 0.001; NS = non-significant
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    Cell viability, cytotoxicity and cell cycle progression in TfRCC cell lines treated with mTOR inhibitors. a , b Cell viability, as measured by MTT assay for TfRCC cell lines and the benign renal epithelial cell line HRCE after 72 h of treatment with up to 1000 nM concentrations of the dual mTORC1/2 inhibitor, AZD8055 ( a ), or selective mTORC1 inhibitor, sirolimus ( b ). Viability in TfRCC cells was suppressed by approximately 80–90% with AZD8055 and 30–50% with sirolimus relative to the untreated (0 nM drug) condition. Both drugs inhibited growth to a greater degree in TfRCC cells than in benign renal cells. c , d Cell cytotoxicity, as measured by LDH release by UOK120 and UOK146 TfRCC cell lines after 48 h of treatment with 1 μM of AZD8055 ( c ) or sirolimus ( d ). Only slight cytotoxicity in UOK120 cells and no cytotoxicity in UOK146 cells was observed after AZD8055 treatment, while sirolimus treatment had no cytotoxic effect. Multi protein inhibitor LY294002 [100 μM] was used as a positive control. e , f Relative fraction of cells in S-phase of the cell cycle, as measured by BrdU incorporation in UOK120 ( e ) and UOK146 ( f ) cell lines treated for 24 h with low (50 nM) and high (500 nM) concentrations of AZD8055 or sirolimus. Dose-dependent reductions in S-phase in both cell lines with either drug mirror the magnitude of reductions observed in cell viability ( a , b ), supporting a predominantly cytostatic mechanism of growth inhibition for both drugs. * p < 0.05; ** p < 0.01; *** p < 0.001; NS = non-significant

    Journal: BMC Cancer

    Article Title: Preclinical efficacy of dual mTORC1/2 inhibitor AZD8055 in renal cell carcinoma harboring a TFE3 gene fusion

    doi: 10.1186/s12885-019-6096-0

    Figure Lengend Snippet: Cell viability, cytotoxicity and cell cycle progression in TfRCC cell lines treated with mTOR inhibitors. a , b Cell viability, as measured by MTT assay for TfRCC cell lines and the benign renal epithelial cell line HRCE after 72 h of treatment with up to 1000 nM concentrations of the dual mTORC1/2 inhibitor, AZD8055 ( a ), or selective mTORC1 inhibitor, sirolimus ( b ). Viability in TfRCC cells was suppressed by approximately 80–90% with AZD8055 and 30–50% with sirolimus relative to the untreated (0 nM drug) condition. Both drugs inhibited growth to a greater degree in TfRCC cells than in benign renal cells. c , d Cell cytotoxicity, as measured by LDH release by UOK120 and UOK146 TfRCC cell lines after 48 h of treatment with 1 μM of AZD8055 ( c ) or sirolimus ( d ). Only slight cytotoxicity in UOK120 cells and no cytotoxicity in UOK146 cells was observed after AZD8055 treatment, while sirolimus treatment had no cytotoxic effect. Multi protein inhibitor LY294002 [100 μM] was used as a positive control. e , f Relative fraction of cells in S-phase of the cell cycle, as measured by BrdU incorporation in UOK120 ( e ) and UOK146 ( f ) cell lines treated for 24 h with low (50 nM) and high (500 nM) concentrations of AZD8055 or sirolimus. Dose-dependent reductions in S-phase in both cell lines with either drug mirror the magnitude of reductions observed in cell viability ( a , b ), supporting a predominantly cytostatic mechanism of growth inhibition for both drugs. * p < 0.05; ** p < 0.01; *** p < 0.001; NS = non-significant

    Article Snippet: RCC4 was obtained from ECACC General Cell Collection (Salisbury, UK; Cat Nr. 03112702) and the human renal cortical epithelial (HRCE) cell line was obtained from ATCC (Manassas, VA; Cat Nr. PCS-400-011).

    Techniques: MTT Assay, Positive Control, BrdU Incorporation Assay, Inhibition