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human tnbc cell lines  (ATCC)


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    ATCC human tnbc cell lines
    Evaluation of FOXM1 protein expression levels and the dose‐dependent inhibitory effects of compound C11 on <t>TNBC</t> cell <t>lines</t> <t>(MDA‐MB‐231</t> and BT‐549). Statistically significance was determined using one‐way ANOVA, with significance levels indicated as follows: ** = p ≤ 0.01, *** = p ≤ 0.001 **** = p ≤ 0.0001 compared to the DMSO control.
    Human Tnbc Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 2952 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/tnbc+cell+lines+bt+549/pmc13135722-498-1-11?v=ATCC
    Average 99 stars, based on 2952 article reviews
    human tnbc cell lines - by Bioz Stars, 2026-08
    99/100 stars

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    1) Product Images from "Design, Synthesis, Biological Evaluation, and Molecular Modeling Studies of Novel 2‐Aminothiazole Derivatives as Potential FOXM1 Inhibitors for Triple‐Negative Breast Cancer Therapy and Structure‐Activity Relationship"

    Article Title: Design, Synthesis, Biological Evaluation, and Molecular Modeling Studies of Novel 2‐Aminothiazole Derivatives as Potential FOXM1 Inhibitors for Triple‐Negative Breast Cancer Therapy and Structure‐Activity Relationship

    Journal: Drug Development Research

    doi: 10.1002/ddr.70296

    Evaluation of FOXM1 protein expression levels and the dose‐dependent inhibitory effects of compound C11 on TNBC cell lines (MDA‐MB‐231 and BT‐549). Statistically significance was determined using one‐way ANOVA, with significance levels indicated as follows: ** = p ≤ 0.01, *** = p ≤ 0.001 **** = p ≤ 0.0001 compared to the DMSO control.
    Figure Legend Snippet: Evaluation of FOXM1 protein expression levels and the dose‐dependent inhibitory effects of compound C11 on TNBC cell lines (MDA‐MB‐231 and BT‐549). Statistically significance was determined using one‐way ANOVA, with significance levels indicated as follows: ** = p ≤ 0.01, *** = p ≤ 0.001 **** = p ≤ 0.0001 compared to the DMSO control.

    Techniques Used: Expressing, Control



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    Evaluation of FOXM1 protein expression levels and the dose‐dependent inhibitory effects of compound C11 on <t>TNBC</t> cell <t>lines</t> <t>(MDA‐MB‐231</t> and BT‐549). Statistically significance was determined using one‐way ANOVA, with significance levels indicated as follows: ** = p ≤ 0.01, *** = p ≤ 0.001 **** = p ≤ 0.0001 compared to the DMSO control.
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    Evaluation of FOXM1 protein expression levels and the dose‐dependent inhibitory effects of compound C11 on <t>TNBC</t> cell <t>lines</t> <t>(MDA‐MB‐231</t> and BT‐549). Statistically significance was determined using one‐way ANOVA, with significance levels indicated as follows: ** = p ≤ 0.01, *** = p ≤ 0.001 **** = p ≤ 0.0001 compared to the DMSO control.
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    G4 is crucial to recruit APE1 to the CXCL1 gene promoter. ( A ) Schematic overview of CRISPR/Cas9-mediated generation of knock-in mutations in the CXCL1 promoter G4 sequence; the WT CXCL1 G4 sequence and mutated G4 sequences are shown (left panel). Sanger sequencing confirmed the homologous mutations (in both alleles) in CXCL1 G4 sequence ( CXCL1 -G4 Mut) compared with the CXCL1 -G4 WT sequence (right panel). ( B ) Enrichment of folded G4 structure in the CXCL1 mutated G4 ( CXCL1 -G4 Mut) promoter versus the CXCL1 WT G4 promoter region in MDA-MB-231 <t>and</t> <t>BT-549</t> cells was examined by promoter-directed ChIP assay with G4-specific antibody. ( C ) Promoter-directed ChIP assay with APE1 antibody in TNBC cells shows enrichment of APE1 in the CXCL1 -G4 WT promoter region and the CXCL1 -G4 Mut promoter. ( D ) Quantitation of CXCL1 expression in TNBC cells containing the CXCL1 -G4 WT and CXCL1 -G4 Mut promoter by qRT-PCR. * P < 0.05; ** P < 0.01; *** P < 0.001, Student’s t -test.
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    G4 is crucial to recruit APE1 to the CXCL1 gene promoter. ( A ) Schematic overview of CRISPR/Cas9-mediated generation of knock-in mutations in the CXCL1 promoter G4 sequence; the WT CXCL1 G4 sequence and mutated G4 sequences are shown (left panel). Sanger sequencing confirmed the homologous mutations (in both alleles) in CXCL1 G4 sequence ( CXCL1 -G4 Mut) compared with the CXCL1 -G4 WT sequence (right panel). ( B ) Enrichment of folded G4 structure in the CXCL1 mutated G4 ( CXCL1 -G4 Mut) promoter versus the CXCL1 WT G4 promoter region in MDA-MB-231 <t>and</t> <t>BT-549</t> cells was examined by promoter-directed ChIP assay with G4-specific antibody. ( C ) Promoter-directed ChIP assay with APE1 antibody in TNBC cells shows enrichment of APE1 in the CXCL1 -G4 WT promoter region and the CXCL1 -G4 Mut promoter. ( D ) Quantitation of CXCL1 expression in TNBC cells containing the CXCL1 -G4 WT and CXCL1 -G4 Mut promoter by qRT-PCR. * P < 0.05; ** P < 0.01; *** P < 0.001, Student’s t -test.
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    G4 is crucial to recruit APE1 to the CXCL1 gene promoter. ( A ) Schematic overview of CRISPR/Cas9-mediated generation of knock-in mutations in the CXCL1 promoter G4 sequence; the WT CXCL1 G4 sequence and mutated G4 sequences are shown (left panel). Sanger sequencing confirmed the homologous mutations (in both alleles) in CXCL1 G4 sequence ( CXCL1 -G4 Mut) compared with the CXCL1 -G4 WT sequence (right panel). ( B ) Enrichment of folded G4 structure in the CXCL1 mutated G4 ( CXCL1 -G4 Mut) promoter versus the CXCL1 WT G4 promoter region in MDA-MB-231 <t>and</t> <t>BT-549</t> cells was examined by promoter-directed ChIP assay with G4-specific antibody. ( C ) Promoter-directed ChIP assay with APE1 antibody in TNBC cells shows enrichment of APE1 in the CXCL1 -G4 WT promoter region and the CXCL1 -G4 Mut promoter. ( D ) Quantitation of CXCL1 expression in TNBC cells containing the CXCL1 -G4 WT and CXCL1 -G4 Mut promoter by qRT-PCR. * P < 0.05; ** P < 0.01; *** P < 0.001, Student’s t -test.
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    G4 is crucial to recruit APE1 to the CXCL1 gene promoter. ( A ) Schematic overview of CRISPR/Cas9-mediated generation of knock-in mutations in the CXCL1 promoter G4 sequence; the WT CXCL1 G4 sequence and mutated G4 sequences are shown (left panel). Sanger sequencing confirmed the homologous mutations (in both alleles) in CXCL1 G4 sequence ( CXCL1 -G4 Mut) compared with the CXCL1 -G4 WT sequence (right panel). ( B ) Enrichment of folded G4 structure in the CXCL1 mutated G4 ( CXCL1 -G4 Mut) promoter versus the CXCL1 WT G4 promoter region in MDA-MB-231 <t>and</t> <t>BT-549</t> cells was examined by promoter-directed ChIP assay with G4-specific antibody. ( C ) Promoter-directed ChIP assay with APE1 antibody in TNBC cells shows enrichment of APE1 in the CXCL1 -G4 WT promoter region and the CXCL1 -G4 Mut promoter. ( D ) Quantitation of CXCL1 expression in TNBC cells containing the CXCL1 -G4 WT and CXCL1 -G4 Mut promoter by qRT-PCR. * P < 0.05; ** P < 0.01; *** P < 0.001, Student’s t -test.
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    G4 is crucial to recruit APE1 to the CXCL1 gene promoter. ( A ) Schematic overview of CRISPR/Cas9-mediated generation of knock-in mutations in the CXCL1 promoter G4 sequence; the WT CXCL1 G4 sequence and mutated G4 sequences are shown (left panel). Sanger sequencing confirmed the homologous mutations (in both alleles) in CXCL1 G4 sequence ( CXCL1 -G4 Mut) compared with the CXCL1 -G4 WT sequence (right panel). ( B ) Enrichment of folded G4 structure in the CXCL1 mutated G4 ( CXCL1 -G4 Mut) promoter versus the CXCL1 WT G4 promoter region in MDA-MB-231 <t>and</t> <t>BT-549</t> cells was examined by promoter-directed ChIP assay with G4-specific antibody. ( C ) Promoter-directed ChIP assay with APE1 antibody in TNBC cells shows enrichment of APE1 in the CXCL1 -G4 WT promoter region and the CXCL1 -G4 Mut promoter. ( D ) Quantitation of CXCL1 expression in TNBC cells containing the CXCL1 -G4 WT and CXCL1 -G4 Mut promoter by qRT-PCR. * P < 0.05; ** P < 0.01; *** P < 0.001, Student’s t -test.
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    Evaluation of FOXM1 protein expression levels and the dose‐dependent inhibitory effects of compound C11 on TNBC cell lines (MDA‐MB‐231 and BT‐549). Statistically significance was determined using one‐way ANOVA, with significance levels indicated as follows: ** = p ≤ 0.01, *** = p ≤ 0.001 **** = p ≤ 0.0001 compared to the DMSO control.

    Journal: Drug Development Research

    Article Title: Design, Synthesis, Biological Evaluation, and Molecular Modeling Studies of Novel 2‐Aminothiazole Derivatives as Potential FOXM1 Inhibitors for Triple‐Negative Breast Cancer Therapy and Structure‐Activity Relationship

    doi: 10.1002/ddr.70296

    Figure Lengend Snippet: Evaluation of FOXM1 protein expression levels and the dose‐dependent inhibitory effects of compound C11 on TNBC cell lines (MDA‐MB‐231 and BT‐549). Statistically significance was determined using one‐way ANOVA, with significance levels indicated as follows: ** = p ≤ 0.01, *** = p ≤ 0.001 **** = p ≤ 0.0001 compared to the DMSO control.

    Article Snippet: The human TNBC cell lines (BT‐549, BT‐20 and MDA‐MB‐231) from the American Type Culture Collection (ATCC, Manassas, VA, USA) were used.

    Techniques: Expressing, Control

    G4 is crucial to recruit APE1 to the CXCL1 gene promoter. ( A ) Schematic overview of CRISPR/Cas9-mediated generation of knock-in mutations in the CXCL1 promoter G4 sequence; the WT CXCL1 G4 sequence and mutated G4 sequences are shown (left panel). Sanger sequencing confirmed the homologous mutations (in both alleles) in CXCL1 G4 sequence ( CXCL1 -G4 Mut) compared with the CXCL1 -G4 WT sequence (right panel). ( B ) Enrichment of folded G4 structure in the CXCL1 mutated G4 ( CXCL1 -G4 Mut) promoter versus the CXCL1 WT G4 promoter region in MDA-MB-231 and BT-549 cells was examined by promoter-directed ChIP assay with G4-specific antibody. ( C ) Promoter-directed ChIP assay with APE1 antibody in TNBC cells shows enrichment of APE1 in the CXCL1 -G4 WT promoter region and the CXCL1 -G4 Mut promoter. ( D ) Quantitation of CXCL1 expression in TNBC cells containing the CXCL1 -G4 WT and CXCL1 -G4 Mut promoter by qRT-PCR. * P < 0.05; ** P < 0.01; *** P < 0.001, Student’s t -test.

    Journal: Nucleic Acids Research

    Article Title: Endogenous promoter G-quadruplexes scaffold apurinic/apyrimidinic endonuclease (APE1) to drive gene expression

    doi: 10.1093/nar/gkag284

    Figure Lengend Snippet: G4 is crucial to recruit APE1 to the CXCL1 gene promoter. ( A ) Schematic overview of CRISPR/Cas9-mediated generation of knock-in mutations in the CXCL1 promoter G4 sequence; the WT CXCL1 G4 sequence and mutated G4 sequences are shown (left panel). Sanger sequencing confirmed the homologous mutations (in both alleles) in CXCL1 G4 sequence ( CXCL1 -G4 Mut) compared with the CXCL1 -G4 WT sequence (right panel). ( B ) Enrichment of folded G4 structure in the CXCL1 mutated G4 ( CXCL1 -G4 Mut) promoter versus the CXCL1 WT G4 promoter region in MDA-MB-231 and BT-549 cells was examined by promoter-directed ChIP assay with G4-specific antibody. ( C ) Promoter-directed ChIP assay with APE1 antibody in TNBC cells shows enrichment of APE1 in the CXCL1 -G4 WT promoter region and the CXCL1 -G4 Mut promoter. ( D ) Quantitation of CXCL1 expression in TNBC cells containing the CXCL1 -G4 WT and CXCL1 -G4 Mut promoter by qRT-PCR. * P < 0.05; ** P < 0.01; *** P < 0.001, Student’s t -test.

    Article Snippet: MDA-MB-231 (HTB-26) and BT-549 (HTB-122) TNBC cell lines were purchased from the ATCC.

    Techniques: CRISPR, Knock-In, Sequencing, Quantitation Assay, Expressing, Quantitative RT-PCR