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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 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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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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ATCC breast cancer 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.
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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.
Bt 549 Htb 122 Tnbc Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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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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ATCC cancer cell lines
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.
Cancer Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Elabscience Biotechnology a549 cells
PC influences the cytotoxicity of NDs. (a) Bright field images of <t>A549</t> cells before and after exposure to oxDND and HPHT ND, with and without PC. (b) Survival rate of A549 cells before and after exposure to NDs, with and without PC, measured using the CCK-8 assay ( n = 3; * p < 0.05).
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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

PC influences the cytotoxicity of NDs. (a) Bright field images of A549 cells before and after exposure to oxDND and HPHT ND, with and without PC. (b) Survival rate of A549 cells before and after exposure to NDs, with and without PC, measured using the CCK-8 assay ( n = 3; * p < 0.05).

Journal: Langmuir

Article Title: Profiling High-Abundance Serum Proteins in the Corona of Nanodiamonds Using Mass Spectrometry

doi: 10.1021/acs.langmuir.5c06674

Figure Lengend Snippet: PC influences the cytotoxicity of NDs. (a) Bright field images of A549 cells before and after exposure to oxDND and HPHT ND, with and without PC. (b) Survival rate of A549 cells before and after exposure to NDs, with and without PC, measured using the CCK-8 assay ( n = 3; * p < 0.05).

Article Snippet: The viability of A549 cells exposed to NDs, with and without PC, was determined using the CCK-8 assay (Elabscience, Japan).

Techniques: CCK-8 Assay