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pharyngeal squamous cell carcinoma cell line fadu  (ATCC)


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    ATCC pharyngeal squamous cell carcinoma cell line fadu
    NF-κB signaling activation promotes LUZP1 expression in HNSCC cells. (A) The expression of LUZP1 in <t>FaDu,</t> OECM-1 and SAS cells treated with SB431542 (10 µM), LY294002 (10 µM), Rapamycin (10 µM), BAY 11–7085 (5 µM) or YC-1 (30 µM) was determined by western blot assay. Signal quantification was measured using ImageJ 1.54 g software (National Institutes of Health) and the relative intensity was normalized to untreated control. The red dashed line represents the normalized value as 1. (B) The expression of LUZP1 in FaDu, OECM-1 and SAS cells with or without BAY 11–7085 was validated by western blot assay. (C) Spearman's monotonic correlation between LUZP1 and NFKB1 or NFKB2 expression in HNSCC was analyzed using The Cancer Genome Atlas RNA-Sequencing database on the GEPIA server. (D) Protein expression of NF-κB p65 and LUZP1 in OECM-1 and SAS cells with NF-κB p65 knockdown (+) or control shRNA -), as determined by western blot analysis. β-actin, loading control. (E) IC 50 values of docetaxel in OECM-1 and SAS cells with or without NF-κB p65 knockdown. (F) IC 50 values of cisplatin in OECM-1 and SAS cells with or without NF-κB p65 knockdown. The expression of LUZP1 in different HNSCC cells treated with (G) IL-1β (3 ng/ml) or (H) TNFα (10 ng/ml) for the indicated times was determined by western blot assay. β-actin, loading control. (I) Transwell cell migration assay was conducted using OECM-1 cells with or without LUZP1 knockdown in the presence or absence of TNFα (10 ng/ml) treatment. Signal quantification using crystal violet extract was measured by colorimetric analysis at 570 nm, and the relative signal intensities were normalized to untreated shControl (shLUZP1, -; TNFα, -) (n=3). (J) Genomic visualization of the human LUZP1 locus (GRCh38/hg38) showing RefSeq-curated exon annotations, NF-κB RelA ChIP-seq binding signals in FaDu cells (ReMap), layered H3K27ac ChIP-seq profiles from ENCODE cell lines, and GeneHancer regulatory element annotations. Red boxes denote promoter regions and gray boxes indicate putative enhancers. Blue vertical bars mark the locations of ChIP-qPCR primer sets designed for experimental validation. (K) ChIP-qPCR analysis showing increased NF-κB (RelA) occupancy at the LUZP1 promoter in response to TNF-α treatment. For statistical analyses, (E and F) a 2-tailed unpaired Student's t -test; (I) a factorial two-way ANOVA, followed by Tukey's Honestly Significant Difference post hoc test. **P<0.01. TPM, transcripts per million; ChIP-seq, chromatin immunoprecipitation sequencing; LUZP1, leucine zipper protein 1; sh, short hairpin.
    Pharyngeal Squamous Cell Carcinoma Cell Line Fadu, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1816 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/squamous+cell+carcinoma+cell+lines/pmc13107151-120-2-16?v=ATCC
    Average 97 stars, based on 1816 article reviews
    pharyngeal squamous cell carcinoma cell line fadu - by Bioz Stars, 2026-07
    97/100 stars

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    1) Product Images from "NF-κB-driven LUZP1 promotes metastasis and chemoresistance in head and neck squamous cell carcinoma"

    Article Title: NF-κB-driven LUZP1 promotes metastasis and chemoresistance in head and neck squamous cell carcinoma

    Journal: Oncology Reports

    doi: 10.3892/or.2026.9115

    NF-κB signaling activation promotes LUZP1 expression in HNSCC cells. (A) The expression of LUZP1 in FaDu, OECM-1 and SAS cells treated with SB431542 (10 µM), LY294002 (10 µM), Rapamycin (10 µM), BAY 11–7085 (5 µM) or YC-1 (30 µM) was determined by western blot assay. Signal quantification was measured using ImageJ 1.54 g software (National Institutes of Health) and the relative intensity was normalized to untreated control. The red dashed line represents the normalized value as 1. (B) The expression of LUZP1 in FaDu, OECM-1 and SAS cells with or without BAY 11–7085 was validated by western blot assay. (C) Spearman's monotonic correlation between LUZP1 and NFKB1 or NFKB2 expression in HNSCC was analyzed using The Cancer Genome Atlas RNA-Sequencing database on the GEPIA server. (D) Protein expression of NF-κB p65 and LUZP1 in OECM-1 and SAS cells with NF-κB p65 knockdown (+) or control shRNA -), as determined by western blot analysis. β-actin, loading control. (E) IC 50 values of docetaxel in OECM-1 and SAS cells with or without NF-κB p65 knockdown. (F) IC 50 values of cisplatin in OECM-1 and SAS cells with or without NF-κB p65 knockdown. The expression of LUZP1 in different HNSCC cells treated with (G) IL-1β (3 ng/ml) or (H) TNFα (10 ng/ml) for the indicated times was determined by western blot assay. β-actin, loading control. (I) Transwell cell migration assay was conducted using OECM-1 cells with or without LUZP1 knockdown in the presence or absence of TNFα (10 ng/ml) treatment. Signal quantification using crystal violet extract was measured by colorimetric analysis at 570 nm, and the relative signal intensities were normalized to untreated shControl (shLUZP1, -; TNFα, -) (n=3). (J) Genomic visualization of the human LUZP1 locus (GRCh38/hg38) showing RefSeq-curated exon annotations, NF-κB RelA ChIP-seq binding signals in FaDu cells (ReMap), layered H3K27ac ChIP-seq profiles from ENCODE cell lines, and GeneHancer regulatory element annotations. Red boxes denote promoter regions and gray boxes indicate putative enhancers. Blue vertical bars mark the locations of ChIP-qPCR primer sets designed for experimental validation. (K) ChIP-qPCR analysis showing increased NF-κB (RelA) occupancy at the LUZP1 promoter in response to TNF-α treatment. For statistical analyses, (E and F) a 2-tailed unpaired Student's t -test; (I) a factorial two-way ANOVA, followed by Tukey's Honestly Significant Difference post hoc test. **P<0.01. TPM, transcripts per million; ChIP-seq, chromatin immunoprecipitation sequencing; LUZP1, leucine zipper protein 1; sh, short hairpin.
    Figure Legend Snippet: NF-κB signaling activation promotes LUZP1 expression in HNSCC cells. (A) The expression of LUZP1 in FaDu, OECM-1 and SAS cells treated with SB431542 (10 µM), LY294002 (10 µM), Rapamycin (10 µM), BAY 11–7085 (5 µM) or YC-1 (30 µM) was determined by western blot assay. Signal quantification was measured using ImageJ 1.54 g software (National Institutes of Health) and the relative intensity was normalized to untreated control. The red dashed line represents the normalized value as 1. (B) The expression of LUZP1 in FaDu, OECM-1 and SAS cells with or without BAY 11–7085 was validated by western blot assay. (C) Spearman's monotonic correlation between LUZP1 and NFKB1 or NFKB2 expression in HNSCC was analyzed using The Cancer Genome Atlas RNA-Sequencing database on the GEPIA server. (D) Protein expression of NF-κB p65 and LUZP1 in OECM-1 and SAS cells with NF-κB p65 knockdown (+) or control shRNA -), as determined by western blot analysis. β-actin, loading control. (E) IC 50 values of docetaxel in OECM-1 and SAS cells with or without NF-κB p65 knockdown. (F) IC 50 values of cisplatin in OECM-1 and SAS cells with or without NF-κB p65 knockdown. The expression of LUZP1 in different HNSCC cells treated with (G) IL-1β (3 ng/ml) or (H) TNFα (10 ng/ml) for the indicated times was determined by western blot assay. β-actin, loading control. (I) Transwell cell migration assay was conducted using OECM-1 cells with or without LUZP1 knockdown in the presence or absence of TNFα (10 ng/ml) treatment. Signal quantification using crystal violet extract was measured by colorimetric analysis at 570 nm, and the relative signal intensities were normalized to untreated shControl (shLUZP1, -; TNFα, -) (n=3). (J) Genomic visualization of the human LUZP1 locus (GRCh38/hg38) showing RefSeq-curated exon annotations, NF-κB RelA ChIP-seq binding signals in FaDu cells (ReMap), layered H3K27ac ChIP-seq profiles from ENCODE cell lines, and GeneHancer regulatory element annotations. Red boxes denote promoter regions and gray boxes indicate putative enhancers. Blue vertical bars mark the locations of ChIP-qPCR primer sets designed for experimental validation. (K) ChIP-qPCR analysis showing increased NF-κB (RelA) occupancy at the LUZP1 promoter in response to TNF-α treatment. For statistical analyses, (E and F) a 2-tailed unpaired Student's t -test; (I) a factorial two-way ANOVA, followed by Tukey's Honestly Significant Difference post hoc test. **P<0.01. TPM, transcripts per million; ChIP-seq, chromatin immunoprecipitation sequencing; LUZP1, leucine zipper protein 1; sh, short hairpin.

    Techniques Used: Activation Assay, Expressing, Western Blot, Software, Control, RNA Sequencing, Knockdown, shRNA, Cell Migration Assay, ChIP-sequencing, Binding Assay, ChIP-qPCR, Biomarker Discovery



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    NF-κB signaling activation promotes LUZP1 expression in HNSCC cells. (A) The expression of LUZP1 in <t>FaDu,</t> OECM-1 and SAS cells treated with SB431542 (10 µM), LY294002 (10 µM), Rapamycin (10 µM), BAY 11–7085 (5 µM) or YC-1 (30 µM) was determined by western blot assay. Signal quantification was measured using ImageJ 1.54 g software (National Institutes of Health) and the relative intensity was normalized to untreated control. The red dashed line represents the normalized value as 1. (B) The expression of LUZP1 in FaDu, OECM-1 and SAS cells with or without BAY 11–7085 was validated by western blot assay. (C) Spearman's monotonic correlation between LUZP1 and NFKB1 or NFKB2 expression in HNSCC was analyzed using The Cancer Genome Atlas RNA-Sequencing database on the GEPIA server. (D) Protein expression of NF-κB p65 and LUZP1 in OECM-1 and SAS cells with NF-κB p65 knockdown (+) or control shRNA -), as determined by western blot analysis. β-actin, loading control. (E) IC 50 values of docetaxel in OECM-1 and SAS cells with or without NF-κB p65 knockdown. (F) IC 50 values of cisplatin in OECM-1 and SAS cells with or without NF-κB p65 knockdown. The expression of LUZP1 in different HNSCC cells treated with (G) IL-1β (3 ng/ml) or (H) TNFα (10 ng/ml) for the indicated times was determined by western blot assay. β-actin, loading control. (I) Transwell cell migration assay was conducted using OECM-1 cells with or without LUZP1 knockdown in the presence or absence of TNFα (10 ng/ml) treatment. Signal quantification using crystal violet extract was measured by colorimetric analysis at 570 nm, and the relative signal intensities were normalized to untreated shControl (shLUZP1, -; TNFα, -) (n=3). (J) Genomic visualization of the human LUZP1 locus (GRCh38/hg38) showing RefSeq-curated exon annotations, NF-κB RelA ChIP-seq binding signals in FaDu cells (ReMap), layered H3K27ac ChIP-seq profiles from ENCODE cell lines, and GeneHancer regulatory element annotations. Red boxes denote promoter regions and gray boxes indicate putative enhancers. Blue vertical bars mark the locations of ChIP-qPCR primer sets designed for experimental validation. (K) ChIP-qPCR analysis showing increased NF-κB (RelA) occupancy at the LUZP1 promoter in response to TNF-α treatment. For statistical analyses, (E and F) a 2-tailed unpaired Student's t -test; (I) a factorial two-way ANOVA, followed by Tukey's Honestly Significant Difference post hoc test. **P<0.01. TPM, transcripts per million; ChIP-seq, chromatin immunoprecipitation sequencing; LUZP1, leucine zipper protein 1; sh, short hairpin.
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    Image Search Results


    NF-κB signaling activation promotes LUZP1 expression in HNSCC cells. (A) The expression of LUZP1 in FaDu, OECM-1 and SAS cells treated with SB431542 (10 µM), LY294002 (10 µM), Rapamycin (10 µM), BAY 11–7085 (5 µM) or YC-1 (30 µM) was determined by western blot assay. Signal quantification was measured using ImageJ 1.54 g software (National Institutes of Health) and the relative intensity was normalized to untreated control. The red dashed line represents the normalized value as 1. (B) The expression of LUZP1 in FaDu, OECM-1 and SAS cells with or without BAY 11–7085 was validated by western blot assay. (C) Spearman's monotonic correlation between LUZP1 and NFKB1 or NFKB2 expression in HNSCC was analyzed using The Cancer Genome Atlas RNA-Sequencing database on the GEPIA server. (D) Protein expression of NF-κB p65 and LUZP1 in OECM-1 and SAS cells with NF-κB p65 knockdown (+) or control shRNA -), as determined by western blot analysis. β-actin, loading control. (E) IC 50 values of docetaxel in OECM-1 and SAS cells with or without NF-κB p65 knockdown. (F) IC 50 values of cisplatin in OECM-1 and SAS cells with or without NF-κB p65 knockdown. The expression of LUZP1 in different HNSCC cells treated with (G) IL-1β (3 ng/ml) or (H) TNFα (10 ng/ml) for the indicated times was determined by western blot assay. β-actin, loading control. (I) Transwell cell migration assay was conducted using OECM-1 cells with or without LUZP1 knockdown in the presence or absence of TNFα (10 ng/ml) treatment. Signal quantification using crystal violet extract was measured by colorimetric analysis at 570 nm, and the relative signal intensities were normalized to untreated shControl (shLUZP1, -; TNFα, -) (n=3). (J) Genomic visualization of the human LUZP1 locus (GRCh38/hg38) showing RefSeq-curated exon annotations, NF-κB RelA ChIP-seq binding signals in FaDu cells (ReMap), layered H3K27ac ChIP-seq profiles from ENCODE cell lines, and GeneHancer regulatory element annotations. Red boxes denote promoter regions and gray boxes indicate putative enhancers. Blue vertical bars mark the locations of ChIP-qPCR primer sets designed for experimental validation. (K) ChIP-qPCR analysis showing increased NF-κB (RelA) occupancy at the LUZP1 promoter in response to TNF-α treatment. For statistical analyses, (E and F) a 2-tailed unpaired Student's t -test; (I) a factorial two-way ANOVA, followed by Tukey's Honestly Significant Difference post hoc test. **P<0.01. TPM, transcripts per million; ChIP-seq, chromatin immunoprecipitation sequencing; LUZP1, leucine zipper protein 1; sh, short hairpin.

    Journal: Oncology Reports

    Article Title: NF-κB-driven LUZP1 promotes metastasis and chemoresistance in head and neck squamous cell carcinoma

    doi: 10.3892/or.2026.9115

    Figure Lengend Snippet: NF-κB signaling activation promotes LUZP1 expression in HNSCC cells. (A) The expression of LUZP1 in FaDu, OECM-1 and SAS cells treated with SB431542 (10 µM), LY294002 (10 µM), Rapamycin (10 µM), BAY 11–7085 (5 µM) or YC-1 (30 µM) was determined by western blot assay. Signal quantification was measured using ImageJ 1.54 g software (National Institutes of Health) and the relative intensity was normalized to untreated control. The red dashed line represents the normalized value as 1. (B) The expression of LUZP1 in FaDu, OECM-1 and SAS cells with or without BAY 11–7085 was validated by western blot assay. (C) Spearman's monotonic correlation between LUZP1 and NFKB1 or NFKB2 expression in HNSCC was analyzed using The Cancer Genome Atlas RNA-Sequencing database on the GEPIA server. (D) Protein expression of NF-κB p65 and LUZP1 in OECM-1 and SAS cells with NF-κB p65 knockdown (+) or control shRNA -), as determined by western blot analysis. β-actin, loading control. (E) IC 50 values of docetaxel in OECM-1 and SAS cells with or without NF-κB p65 knockdown. (F) IC 50 values of cisplatin in OECM-1 and SAS cells with or without NF-κB p65 knockdown. The expression of LUZP1 in different HNSCC cells treated with (G) IL-1β (3 ng/ml) or (H) TNFα (10 ng/ml) for the indicated times was determined by western blot assay. β-actin, loading control. (I) Transwell cell migration assay was conducted using OECM-1 cells with or without LUZP1 knockdown in the presence or absence of TNFα (10 ng/ml) treatment. Signal quantification using crystal violet extract was measured by colorimetric analysis at 570 nm, and the relative signal intensities were normalized to untreated shControl (shLUZP1, -; TNFα, -) (n=3). (J) Genomic visualization of the human LUZP1 locus (GRCh38/hg38) showing RefSeq-curated exon annotations, NF-κB RelA ChIP-seq binding signals in FaDu cells (ReMap), layered H3K27ac ChIP-seq profiles from ENCODE cell lines, and GeneHancer regulatory element annotations. Red boxes denote promoter regions and gray boxes indicate putative enhancers. Blue vertical bars mark the locations of ChIP-qPCR primer sets designed for experimental validation. (K) ChIP-qPCR analysis showing increased NF-κB (RelA) occupancy at the LUZP1 promoter in response to TNF-α treatment. For statistical analyses, (E and F) a 2-tailed unpaired Student's t -test; (I) a factorial two-way ANOVA, followed by Tukey's Honestly Significant Difference post hoc test. **P<0.01. TPM, transcripts per million; ChIP-seq, chromatin immunoprecipitation sequencing; LUZP1, leucine zipper protein 1; sh, short hairpin.

    Article Snippet: The human pharyngeal squamous cell carcinoma cell line FaDu (cat. no. HTB-43) was obtained from the American Type Culture Collection.

    Techniques: Activation Assay, Expressing, Western Blot, Software, Control, RNA Sequencing, Knockdown, shRNA, Cell Migration Assay, ChIP-sequencing, Binding Assay, ChIP-qPCR, Biomarker Discovery

    HMGN1 inhibition affects the proliferation of cervical squamous cells. (A) mRNA and (B) protein expression levels of HMGN1 in SiHa and HeLa cells following siRNA transfection, compared with the NC. (C) Cell Counting Kit-8 assay assessing the proliferation of SiHa and HeLa cells at 24, 48 and 72 h. (D) Cell cycle distribution of SiHa and HeLa cells after HMGN1 inhibition was analyzed by flow cytometry, including flow cytometry plots and quantitative histograms. *P<0.05, **P<0.01 and ****P<0.001. HMGN1, high-mobility group nucleosome-binding protein 1; NC, non-targeting control; si, small interfering RNA.

    Journal: Oncology Letters

    Article Title: Lactylation-based machine algorithm combined with multi-omics analysis to predict prognosis in cervical cancer

    doi: 10.3892/ol.2026.15486

    Figure Lengend Snippet: HMGN1 inhibition affects the proliferation of cervical squamous cells. (A) mRNA and (B) protein expression levels of HMGN1 in SiHa and HeLa cells following siRNA transfection, compared with the NC. (C) Cell Counting Kit-8 assay assessing the proliferation of SiHa and HeLa cells at 24, 48 and 72 h. (D) Cell cycle distribution of SiHa and HeLa cells after HMGN1 inhibition was analyzed by flow cytometry, including flow cytometry plots and quantitative histograms. *P<0.05, **P<0.01 and ****P<0.001. HMGN1, high-mobility group nucleosome-binding protein 1; NC, non-targeting control; si, small interfering RNA.

    Article Snippet: Human cervical squamous cell carcinoma cell lines SiHa (cat. no. HTB-35) and HeLa (cat. no. CRM-CCL-2) were obtained from the American Type Culture Collection and the human keratinocyte cell line HaCaT was obtained from The Cell Bank of Type Culture Collection of the Chinese Academy of Sciences (SCSP-5091; Beijing, China).

    Techniques: Inhibition, Expressing, Transfection, Cell Counting, Flow Cytometry, Binding Assay, Control, Small Interfering RNA

    Mendelian Randomization Analysis Reveals Causal Relationship Between Phosphatidylcholine and Lung Cancer. A and B show meta-analysis forest plots demonstrating that phosphatidylcholine levels are significantly associated with LUSC risk across multiple studies. The red diamonds represent pooled effect estimates. C presents MR test scatter plots using three different methods (inverse variance weighted, MR-Egger, and weighted median). The consistent regression line slopes across methods indicate a robust causal effect estimate. D compares results from different MR methods, with the blue line showing the primary analysis and scattered points representing alternative approaches. The consistency across methods supports the reliability of findings

    Journal: Discover Oncology

    Article Title: Comprehensive multi omics profiling and Mendelian randomization assessment of lipid metabolites in lung cancer prognosis

    doi: 10.1007/s12672-026-04893-6

    Figure Lengend Snippet: Mendelian Randomization Analysis Reveals Causal Relationship Between Phosphatidylcholine and Lung Cancer. A and B show meta-analysis forest plots demonstrating that phosphatidylcholine levels are significantly associated with LUSC risk across multiple studies. The red diamonds represent pooled effect estimates. C presents MR test scatter plots using three different methods (inverse variance weighted, MR-Egger, and weighted median). The consistent regression line slopes across methods indicate a robust causal effect estimate. D compares results from different MR methods, with the blue line showing the primary analysis and scattered points representing alternative approaches. The consistency across methods supports the reliability of findings

    Article Snippet: ATCC-procured H520 and SW900 human lung squamous cell carcinoma (LUSC) cell lines, alongside BEAS-2B normal bronchial epithelial cells, were utilized.

    Techniques:

    Mendelian Randomization Analysis Reveals Associations between LUSC and Metabolites. The charts present Mendelian randomization findings exploring the link between lung cancer and metabolites. A and B illustrate the associations, while C and D confirm consistency. The analysis suggests significant relations between certain metabolites and lung cancer risk, offering new insights for research

    Journal: Discover Oncology

    Article Title: Comprehensive multi omics profiling and Mendelian randomization assessment of lipid metabolites in lung cancer prognosis

    doi: 10.1007/s12672-026-04893-6

    Figure Lengend Snippet: Mendelian Randomization Analysis Reveals Associations between LUSC and Metabolites. The charts present Mendelian randomization findings exploring the link between lung cancer and metabolites. A and B illustrate the associations, while C and D confirm consistency. The analysis suggests significant relations between certain metabolites and lung cancer risk, offering new insights for research

    Article Snippet: ATCC-procured H520 and SW900 human lung squamous cell carcinoma (LUSC) cell lines, alongside BEAS-2B normal bronchial epithelial cells, were utilized.

    Techniques:

    RT-qPCR Validation of Prognostic Genes. Relative mRNA expression of CD44, OR51E2, KRT5, and S100A9 in H520 and SW900 lung squamous cell carcinoma (LUSC) cell lines vs. BEAS-2B controls. *** P < 0.001, **** P < 0.0001

    Journal: Discover Oncology

    Article Title: Comprehensive multi omics profiling and Mendelian randomization assessment of lipid metabolites in lung cancer prognosis

    doi: 10.1007/s12672-026-04893-6

    Figure Lengend Snippet: RT-qPCR Validation of Prognostic Genes. Relative mRNA expression of CD44, OR51E2, KRT5, and S100A9 in H520 and SW900 lung squamous cell carcinoma (LUSC) cell lines vs. BEAS-2B controls. *** P < 0.001, **** P < 0.0001

    Article Snippet: ATCC-procured H520 and SW900 human lung squamous cell carcinoma (LUSC) cell lines, alongside BEAS-2B normal bronchial epithelial cells, were utilized.

    Techniques: Quantitative RT-PCR, Biomarker Discovery, Expressing