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human hpc fadu cells  (ATCC)


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    Structured Review

    ATCC human hpc fadu cells
    Effects of AT-1 on <t>FaDu</t> cells and PDL cells. (A) Cell viability was assessed using the MTT assay after FaDu cells and PDL cells were treated with different concentrations of AT-1 for 24 h. (B) Images of FaDu and PDL cells treated with AT-1 (1 mM) or DMSO for 24 h. Red arrows indicate rounded, mitosis-like cells and yellow arrows indicate unchanged cells for demonstration. Scale bar = 100 μm. (C) Quantification of rounded cells from cell images. (D) Comparison of cell proliferative rates of FaDu cells treated with AT-1 or DMSO. (E) Quantification of intracellular ROS levels using the DCFDA fluorescence assay. Data are normalized to cell viability (mean ± SEM, n = 3). ∗ and #: p < 0.05, ∗∗ and ###: p < 0.005, ##: p < 0.01, ∗∗∗: p < 0.001, and ∗∗∗∗: p < 0.0001 compared to the control group.
    Human Hpc Fadu Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 2029 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 99 stars, based on 2029 article reviews
    human hpc fadu cells - by Bioz Stars, 2026-02
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    Images

    1) Product Images from "8-O-acetylharpagide, an active compound isolated from A. taiwanensis selectively induced G2/M phase arrest and radiosensitivity in hypopharyngeal cancer cells"

    Article Title: 8-O-acetylharpagide, an active compound isolated from A. taiwanensis selectively induced G2/M phase arrest and radiosensitivity in hypopharyngeal cancer cells

    Journal: Biochemistry and Biophysics Reports

    doi: 10.1016/j.bbrep.2025.102431

    Effects of AT-1 on FaDu cells and PDL cells. (A) Cell viability was assessed using the MTT assay after FaDu cells and PDL cells were treated with different concentrations of AT-1 for 24 h. (B) Images of FaDu and PDL cells treated with AT-1 (1 mM) or DMSO for 24 h. Red arrows indicate rounded, mitosis-like cells and yellow arrows indicate unchanged cells for demonstration. Scale bar = 100 μm. (C) Quantification of rounded cells from cell images. (D) Comparison of cell proliferative rates of FaDu cells treated with AT-1 or DMSO. (E) Quantification of intracellular ROS levels using the DCFDA fluorescence assay. Data are normalized to cell viability (mean ± SEM, n = 3). ∗ and #: p < 0.05, ∗∗ and ###: p < 0.005, ##: p < 0.01, ∗∗∗: p < 0.001, and ∗∗∗∗: p < 0.0001 compared to the control group.
    Figure Legend Snippet: Effects of AT-1 on FaDu cells and PDL cells. (A) Cell viability was assessed using the MTT assay after FaDu cells and PDL cells were treated with different concentrations of AT-1 for 24 h. (B) Images of FaDu and PDL cells treated with AT-1 (1 mM) or DMSO for 24 h. Red arrows indicate rounded, mitosis-like cells and yellow arrows indicate unchanged cells for demonstration. Scale bar = 100 μm. (C) Quantification of rounded cells from cell images. (D) Comparison of cell proliferative rates of FaDu cells treated with AT-1 or DMSO. (E) Quantification of intracellular ROS levels using the DCFDA fluorescence assay. Data are normalized to cell viability (mean ± SEM, n = 3). ∗ and #: p < 0.05, ∗∗ and ###: p < 0.005, ##: p < 0.01, ∗∗∗: p < 0.001, and ∗∗∗∗: p < 0.0001 compared to the control group.

    Techniques Used: MTT Assay, Comparison, Fluorescence, Control

    AT-1 induced G2/M phase arrest in FaDu cells but not PDL cells. (A) and (B) Flow cytometric analysis of cell cycle distribution in FaDu cells and PDL cells treated with or without AT-1 for 24 h, respectively. (C) Quantification of cell cycle phases (Sub G1, G0/G1, S, G2/M) in FaDu and PDL cells. Data were presented as mean ± SEM from three independent experiments. (D) Western blot analysis of cell cycles related proteins in FaDu cells and PDL cells treated with AT-1. Cyclin B1, CDK1, p21, and CHK1 protein expression levels were normalized to GAPDH. (E) Summary bar graphs for Western blot quantification (mean ± SEM, n = 3). ∗ and #: p < 0.05, ∗∗ and ###: p < 0.005 compared to the control group.
    Figure Legend Snippet: AT-1 induced G2/M phase arrest in FaDu cells but not PDL cells. (A) and (B) Flow cytometric analysis of cell cycle distribution in FaDu cells and PDL cells treated with or without AT-1 for 24 h, respectively. (C) Quantification of cell cycle phases (Sub G1, G0/G1, S, G2/M) in FaDu and PDL cells. Data were presented as mean ± SEM from three independent experiments. (D) Western blot analysis of cell cycles related proteins in FaDu cells and PDL cells treated with AT-1. Cyclin B1, CDK1, p21, and CHK1 protein expression levels were normalized to GAPDH. (E) Summary bar graphs for Western blot quantification (mean ± SEM, n = 3). ∗ and #: p < 0.05, ∗∗ and ###: p < 0.005 compared to the control group.

    Techniques Used: Western Blot, Expressing, Control

    Effects of AT-1 induced apoptosis in FaDu cells and PDL cells. (A) Flow cytometric profiles of annexin V/PI dual staining in FaDu cells and PDL cells with different treatments for 24 h. (B) and (C) Quantification of necrosis-like, late apoptosis, and early apoptosis in FaDu cells and PDL cells, respectively. (D) Western blot analysis of apoptotic related proteins in FaDu and PDL cells treated with AT-1. AKT, pAKT, and BCL-2 protein expression levels were normalized to GAPDH. (E) Summary bar graphs for Western blot quantification (mean ± SEM, n = 3) ∗: p < 0.05, ∗∗∗∗: p < 0.001.
    Figure Legend Snippet: Effects of AT-1 induced apoptosis in FaDu cells and PDL cells. (A) Flow cytometric profiles of annexin V/PI dual staining in FaDu cells and PDL cells with different treatments for 24 h. (B) and (C) Quantification of necrosis-like, late apoptosis, and early apoptosis in FaDu cells and PDL cells, respectively. (D) Western blot analysis of apoptotic related proteins in FaDu and PDL cells treated with AT-1. AKT, pAKT, and BCL-2 protein expression levels were normalized to GAPDH. (E) Summary bar graphs for Western blot quantification (mean ± SEM, n = 3) ∗: p < 0.05, ∗∗∗∗: p < 0.001.

    Techniques Used: Staining, Western Blot, Expressing

    Effects of AT-1 on radiosensitivity of FaDu cells and PDL cells. (A) and (B) MTT assay for analysis of the cell viability of FaDu cells and PDL cells irradiated with different doses of X-rays after AT-1 treatment, respectively. Cell viability was presented as fractions relative to the control group (0 Gy, set as 1). ∗∗∗∗: p < 0.0001.
    Figure Legend Snippet: Effects of AT-1 on radiosensitivity of FaDu cells and PDL cells. (A) and (B) MTT assay for analysis of the cell viability of FaDu cells and PDL cells irradiated with different doses of X-rays after AT-1 treatment, respectively. Cell viability was presented as fractions relative to the control group (0 Gy, set as 1). ∗∗∗∗: p < 0.0001.

    Techniques Used: MTT Assay, Irradiation, Control



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    ATCC human hpc fadu cells
    Effects of AT-1 on <t>FaDu</t> cells and PDL cells. (A) Cell viability was assessed using the MTT assay after FaDu cells and PDL cells were treated with different concentrations of AT-1 for 24 h. (B) Images of FaDu and PDL cells treated with AT-1 (1 mM) or DMSO for 24 h. Red arrows indicate rounded, mitosis-like cells and yellow arrows indicate unchanged cells for demonstration. Scale bar = 100 μm. (C) Quantification of rounded cells from cell images. (D) Comparison of cell proliferative rates of FaDu cells treated with AT-1 or DMSO. (E) Quantification of intracellular ROS levels using the DCFDA fluorescence assay. Data are normalized to cell viability (mean ± SEM, n = 3). ∗ and #: p < 0.05, ∗∗ and ###: p < 0.005, ##: p < 0.01, ∗∗∗: p < 0.001, and ∗∗∗∗: p < 0.0001 compared to the control group.
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    (A) Kaplan-Meier analysis showing that neutrophil density negatively correlates with patient outcome, n=83 patients. (B) CD66b + TAN were analyzed by immunofluorescence and quantified in tumor, tumor margin and stroma of HNSCC patients (mean ± SD, n=83, circles = males, open circles = females). (C) Schematic overview of the in vitro system for tumor-stroma communication, generated using BioRender. (D) SNs from tumor <t>(FaDu,</t> <t>PCI13),</t> MSC-primed tumor, MSCs and tumor-primed MSCs were analysed for released CXCL8 by ELISA, mean + SD, n=3. (E) The impact of these SN on PMN chemotaxis was analyzed using transwell assays, mean + SD, n=3-8. (F) Luminex screening was performed on SNs from FaDu cells and seven patient-derived MSC lines, analyzed both in their naïve state and after FaDu-priming. CXCL8 was measured using ELISA. Data are depicted in pg/mL. Statistical analysis was performed with Kruskal-Wallis (B) and ordinary one-way ANOVA (D, E). P -values are indicated.
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    fadu  (ATCC)
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    (A) Kaplan-Meier analysis showing that neutrophil density negatively correlates with patient outcome, n=83 patients. (B) CD66b + TAN were analyzed by immunofluorescence and quantified in tumor, tumor margin and stroma of HNSCC patients (mean ± SD, n=83, circles = males, open circles = females). (C) Schematic overview of the in vitro system for tumor-stroma communication, generated using BioRender. (D) SNs from tumor <t>(FaDu,</t> <t>PCI13),</t> MSC-primed tumor, MSCs and tumor-primed MSCs were analysed for released CXCL8 by ELISA, mean + SD, n=3. (E) The impact of these SN on PMN chemotaxis was analyzed using transwell assays, mean + SD, n=3-8. (F) Luminex screening was performed on SNs from FaDu cells and seven patient-derived MSC lines, analyzed both in their naïve state and after FaDu-priming. CXCL8 was measured using ELISA. Data are depicted in pg/mL. Statistical analysis was performed with Kruskal-Wallis (B) and ordinary one-way ANOVA (D, E). P -values are indicated.
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    (A) Kaplan-Meier analysis showing that neutrophil density negatively correlates with patient outcome, n=83 patients. (B) CD66b + TAN were analyzed by immunofluorescence and quantified in tumor, tumor margin and stroma of HNSCC patients (mean ± SD, n=83, circles = males, open circles = females). (C) Schematic overview of the in vitro system for tumor-stroma communication, generated using BioRender. (D) SNs from tumor <t>(FaDu,</t> <t>PCI13),</t> MSC-primed tumor, MSCs and tumor-primed MSCs were analysed for released CXCL8 by ELISA, mean + SD, n=3. (E) The impact of these SN on PMN chemotaxis was analyzed using transwell assays, mean + SD, n=3-8. (F) Luminex screening was performed on SNs from FaDu cells and seven patient-derived MSC lines, analyzed both in their naïve state and after FaDu-priming. CXCL8 was measured using ELISA. Data are depicted in pg/mL. Statistical analysis was performed with Kruskal-Wallis (B) and ordinary one-way ANOVA (D, E). P -values are indicated.
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    Single-cell transcriptomic profiling and validation of CRABP2. (A,B) UMAP plots showing clustering of cells from nine mixed samples (A) and annotation of 11 distinct cell types (B). (C) UMAP plot of epithelial and malignant cells across all samples. (D) Left: differentiation trajectory of epithelial and malignant cells colored by cell state. Middle: Pseudotime trajectory of epithelial cells. Right: stemness score along the epithelial cell trajectory. (E) Differentially expressed genes between cell fate 1 and fate 2. (F) Dynamic expression patterns of DEGs along pseudotime in well- versus poorly differentiated groups. (G) IHC of CRABP2 in well- and poorly differentiated HNSCC tissue samples (n=5 each). Top: representative IHC images (magnification, ×10). Bottom: quantification of stained area and intensity using Image-Pro Plus software. (H) Western blot (left) and RT-PCR (right) showing expression of CRABP2 and differentiation markers (CD44, IVL) following CRABP2 knockdown in <t>FADU</t> <t>cells.</t> (I) Representative images (left) and quantification (right) of cell sphere formation in NC and siCRABP2-treated cells (magnification, ×20). *, P<0.05; **, P<0.01; ***, P<0.001. AOD, average optical density; ; DEGs, differentially expressed genes; HNSCC, head and neck squamous cell carcinoma; IHC, immunohistochemistry; NC, negative control; RT-PCR, reverse transcription polymerase chain reaction; UMAP, Uniform Manifold Approximation and Projection.
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    Single-cell transcriptomic profiling and validation of CRABP2. (A,B) UMAP plots showing clustering of cells from nine mixed samples (A) and annotation of 11 distinct cell types (B). (C) UMAP plot of epithelial and malignant cells across all samples. (D) Left: differentiation trajectory of epithelial and malignant cells colored by cell state. Middle: Pseudotime trajectory of epithelial cells. Right: stemness score along the epithelial cell trajectory. (E) Differentially expressed genes between cell fate 1 and fate 2. (F) Dynamic expression patterns of DEGs along pseudotime in well- versus poorly differentiated groups. (G) IHC of CRABP2 in well- and poorly differentiated HNSCC tissue samples (n=5 each). Top: representative IHC images (magnification, ×10). Bottom: quantification of stained area and intensity using Image-Pro Plus software. (H) Western blot (left) and RT-PCR (right) showing expression of CRABP2 and differentiation markers (CD44, IVL) following CRABP2 knockdown in <t>FADU</t> <t>cells.</t> (I) Representative images (left) and quantification (right) of cell sphere formation in NC and siCRABP2-treated cells (magnification, ×20). *, P<0.05; **, P<0.01; ***, P<0.001. AOD, average optical density; ; DEGs, differentially expressed genes; HNSCC, head and neck squamous cell carcinoma; IHC, immunohistochemistry; NC, negative control; RT-PCR, reverse transcription polymerase chain reaction; UMAP, Uniform Manifold Approximation and Projection.
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    Image Search Results


    Effects of AT-1 on FaDu cells and PDL cells. (A) Cell viability was assessed using the MTT assay after FaDu cells and PDL cells were treated with different concentrations of AT-1 for 24 h. (B) Images of FaDu and PDL cells treated with AT-1 (1 mM) or DMSO for 24 h. Red arrows indicate rounded, mitosis-like cells and yellow arrows indicate unchanged cells for demonstration. Scale bar = 100 μm. (C) Quantification of rounded cells from cell images. (D) Comparison of cell proliferative rates of FaDu cells treated with AT-1 or DMSO. (E) Quantification of intracellular ROS levels using the DCFDA fluorescence assay. Data are normalized to cell viability (mean ± SEM, n = 3). ∗ and #: p < 0.05, ∗∗ and ###: p < 0.005, ##: p < 0.01, ∗∗∗: p < 0.001, and ∗∗∗∗: p < 0.0001 compared to the control group.

    Journal: Biochemistry and Biophysics Reports

    Article Title: 8-O-acetylharpagide, an active compound isolated from A. taiwanensis selectively induced G2/M phase arrest and radiosensitivity in hypopharyngeal cancer cells

    doi: 10.1016/j.bbrep.2025.102431

    Figure Lengend Snippet: Effects of AT-1 on FaDu cells and PDL cells. (A) Cell viability was assessed using the MTT assay after FaDu cells and PDL cells were treated with different concentrations of AT-1 for 24 h. (B) Images of FaDu and PDL cells treated with AT-1 (1 mM) or DMSO for 24 h. Red arrows indicate rounded, mitosis-like cells and yellow arrows indicate unchanged cells for demonstration. Scale bar = 100 μm. (C) Quantification of rounded cells from cell images. (D) Comparison of cell proliferative rates of FaDu cells treated with AT-1 or DMSO. (E) Quantification of intracellular ROS levels using the DCFDA fluorescence assay. Data are normalized to cell viability (mean ± SEM, n = 3). ∗ and #: p < 0.05, ∗∗ and ###: p < 0.005, ##: p < 0.01, ∗∗∗: p < 0.001, and ∗∗∗∗: p < 0.0001 compared to the control group.

    Article Snippet: Human HPC FaDu cells were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA) and maintained in RPMI-1640 medium (Life Technologies, Carlsbad, CA, USA).

    Techniques: MTT Assay, Comparison, Fluorescence, Control

    AT-1 induced G2/M phase arrest in FaDu cells but not PDL cells. (A) and (B) Flow cytometric analysis of cell cycle distribution in FaDu cells and PDL cells treated with or without AT-1 for 24 h, respectively. (C) Quantification of cell cycle phases (Sub G1, G0/G1, S, G2/M) in FaDu and PDL cells. Data were presented as mean ± SEM from three independent experiments. (D) Western blot analysis of cell cycles related proteins in FaDu cells and PDL cells treated with AT-1. Cyclin B1, CDK1, p21, and CHK1 protein expression levels were normalized to GAPDH. (E) Summary bar graphs for Western blot quantification (mean ± SEM, n = 3). ∗ and #: p < 0.05, ∗∗ and ###: p < 0.005 compared to the control group.

    Journal: Biochemistry and Biophysics Reports

    Article Title: 8-O-acetylharpagide, an active compound isolated from A. taiwanensis selectively induced G2/M phase arrest and radiosensitivity in hypopharyngeal cancer cells

    doi: 10.1016/j.bbrep.2025.102431

    Figure Lengend Snippet: AT-1 induced G2/M phase arrest in FaDu cells but not PDL cells. (A) and (B) Flow cytometric analysis of cell cycle distribution in FaDu cells and PDL cells treated with or without AT-1 for 24 h, respectively. (C) Quantification of cell cycle phases (Sub G1, G0/G1, S, G2/M) in FaDu and PDL cells. Data were presented as mean ± SEM from three independent experiments. (D) Western blot analysis of cell cycles related proteins in FaDu cells and PDL cells treated with AT-1. Cyclin B1, CDK1, p21, and CHK1 protein expression levels were normalized to GAPDH. (E) Summary bar graphs for Western blot quantification (mean ± SEM, n = 3). ∗ and #: p < 0.05, ∗∗ and ###: p < 0.005 compared to the control group.

    Article Snippet: Human HPC FaDu cells were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA) and maintained in RPMI-1640 medium (Life Technologies, Carlsbad, CA, USA).

    Techniques: Western Blot, Expressing, Control

    Effects of AT-1 induced apoptosis in FaDu cells and PDL cells. (A) Flow cytometric profiles of annexin V/PI dual staining in FaDu cells and PDL cells with different treatments for 24 h. (B) and (C) Quantification of necrosis-like, late apoptosis, and early apoptosis in FaDu cells and PDL cells, respectively. (D) Western blot analysis of apoptotic related proteins in FaDu and PDL cells treated with AT-1. AKT, pAKT, and BCL-2 protein expression levels were normalized to GAPDH. (E) Summary bar graphs for Western blot quantification (mean ± SEM, n = 3) ∗: p < 0.05, ∗∗∗∗: p < 0.001.

    Journal: Biochemistry and Biophysics Reports

    Article Title: 8-O-acetylharpagide, an active compound isolated from A. taiwanensis selectively induced G2/M phase arrest and radiosensitivity in hypopharyngeal cancer cells

    doi: 10.1016/j.bbrep.2025.102431

    Figure Lengend Snippet: Effects of AT-1 induced apoptosis in FaDu cells and PDL cells. (A) Flow cytometric profiles of annexin V/PI dual staining in FaDu cells and PDL cells with different treatments for 24 h. (B) and (C) Quantification of necrosis-like, late apoptosis, and early apoptosis in FaDu cells and PDL cells, respectively. (D) Western blot analysis of apoptotic related proteins in FaDu and PDL cells treated with AT-1. AKT, pAKT, and BCL-2 protein expression levels were normalized to GAPDH. (E) Summary bar graphs for Western blot quantification (mean ± SEM, n = 3) ∗: p < 0.05, ∗∗∗∗: p < 0.001.

    Article Snippet: Human HPC FaDu cells were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA) and maintained in RPMI-1640 medium (Life Technologies, Carlsbad, CA, USA).

    Techniques: Staining, Western Blot, Expressing

    Effects of AT-1 on radiosensitivity of FaDu cells and PDL cells. (A) and (B) MTT assay for analysis of the cell viability of FaDu cells and PDL cells irradiated with different doses of X-rays after AT-1 treatment, respectively. Cell viability was presented as fractions relative to the control group (0 Gy, set as 1). ∗∗∗∗: p < 0.0001.

    Journal: Biochemistry and Biophysics Reports

    Article Title: 8-O-acetylharpagide, an active compound isolated from A. taiwanensis selectively induced G2/M phase arrest and radiosensitivity in hypopharyngeal cancer cells

    doi: 10.1016/j.bbrep.2025.102431

    Figure Lengend Snippet: Effects of AT-1 on radiosensitivity of FaDu cells and PDL cells. (A) and (B) MTT assay for analysis of the cell viability of FaDu cells and PDL cells irradiated with different doses of X-rays after AT-1 treatment, respectively. Cell viability was presented as fractions relative to the control group (0 Gy, set as 1). ∗∗∗∗: p < 0.0001.

    Article Snippet: Human HPC FaDu cells were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA) and maintained in RPMI-1640 medium (Life Technologies, Carlsbad, CA, USA).

    Techniques: MTT Assay, Irradiation, Control

    (A) Kaplan-Meier analysis showing that neutrophil density negatively correlates with patient outcome, n=83 patients. (B) CD66b + TAN were analyzed by immunofluorescence and quantified in tumor, tumor margin and stroma of HNSCC patients (mean ± SD, n=83, circles = males, open circles = females). (C) Schematic overview of the in vitro system for tumor-stroma communication, generated using BioRender. (D) SNs from tumor (FaDu, PCI13), MSC-primed tumor, MSCs and tumor-primed MSCs were analysed for released CXCL8 by ELISA, mean + SD, n=3. (E) The impact of these SN on PMN chemotaxis was analyzed using transwell assays, mean + SD, n=3-8. (F) Luminex screening was performed on SNs from FaDu cells and seven patient-derived MSC lines, analyzed both in their naïve state and after FaDu-priming. CXCL8 was measured using ELISA. Data are depicted in pg/mL. Statistical analysis was performed with Kruskal-Wallis (B) and ordinary one-way ANOVA (D, E). P -values are indicated.

    Journal: bioRxiv

    Article Title: IL-1α drives a tumor-stroma-neutrophil axis through inflammatory fibroblast activation in head and neck cancer

    doi: 10.64898/2026.01.20.700440

    Figure Lengend Snippet: (A) Kaplan-Meier analysis showing that neutrophil density negatively correlates with patient outcome, n=83 patients. (B) CD66b + TAN were analyzed by immunofluorescence and quantified in tumor, tumor margin and stroma of HNSCC patients (mean ± SD, n=83, circles = males, open circles = females). (C) Schematic overview of the in vitro system for tumor-stroma communication, generated using BioRender. (D) SNs from tumor (FaDu, PCI13), MSC-primed tumor, MSCs and tumor-primed MSCs were analysed for released CXCL8 by ELISA, mean + SD, n=3. (E) The impact of these SN on PMN chemotaxis was analyzed using transwell assays, mean + SD, n=3-8. (F) Luminex screening was performed on SNs from FaDu cells and seven patient-derived MSC lines, analyzed both in their naïve state and after FaDu-priming. CXCL8 was measured using ELISA. Data are depicted in pg/mL. Statistical analysis was performed with Kruskal-Wallis (B) and ordinary one-way ANOVA (D, E). P -values are indicated.

    Article Snippet: The head and neck cancer cell lines FaDu (ATCC HTB-43) and PCI13 (kindly provided by the Pittsburgh Cancer Institute) were cultured in RPMI-1640 (Pan-Biotech), supplemented with 10% FCS (BioSell) and 100 units/mL penicillin and 100 μg/mL streptomycin (Thermo Fisher Scientific, Waltham, USA).

    Techniques: Immunofluorescence, In Vitro, Generated, Enzyme-linked Immunosorbent Assay, Chemotaxis Assay, Luminex, Derivative Assay

    Single-cell transcriptomic profiling and validation of CRABP2. (A,B) UMAP plots showing clustering of cells from nine mixed samples (A) and annotation of 11 distinct cell types (B). (C) UMAP plot of epithelial and malignant cells across all samples. (D) Left: differentiation trajectory of epithelial and malignant cells colored by cell state. Middle: Pseudotime trajectory of epithelial cells. Right: stemness score along the epithelial cell trajectory. (E) Differentially expressed genes between cell fate 1 and fate 2. (F) Dynamic expression patterns of DEGs along pseudotime in well- versus poorly differentiated groups. (G) IHC of CRABP2 in well- and poorly differentiated HNSCC tissue samples (n=5 each). Top: representative IHC images (magnification, ×10). Bottom: quantification of stained area and intensity using Image-Pro Plus software. (H) Western blot (left) and RT-PCR (right) showing expression of CRABP2 and differentiation markers (CD44, IVL) following CRABP2 knockdown in FADU cells. (I) Representative images (left) and quantification (right) of cell sphere formation in NC and siCRABP2-treated cells (magnification, ×20). *, P<0.05; **, P<0.01; ***, P<0.001. AOD, average optical density; ; DEGs, differentially expressed genes; HNSCC, head and neck squamous cell carcinoma; IHC, immunohistochemistry; NC, negative control; RT-PCR, reverse transcription polymerase chain reaction; UMAP, Uniform Manifold Approximation and Projection.

    Journal: Translational Cancer Research

    Article Title: Identification of differentiation markers and immune microenvironment in head and neck squamous cell carcinoma using machine learning combined with single-cell analysis

    doi: 10.21037/tcr-2025-1723

    Figure Lengend Snippet: Single-cell transcriptomic profiling and validation of CRABP2. (A,B) UMAP plots showing clustering of cells from nine mixed samples (A) and annotation of 11 distinct cell types (B). (C) UMAP plot of epithelial and malignant cells across all samples. (D) Left: differentiation trajectory of epithelial and malignant cells colored by cell state. Middle: Pseudotime trajectory of epithelial cells. Right: stemness score along the epithelial cell trajectory. (E) Differentially expressed genes between cell fate 1 and fate 2. (F) Dynamic expression patterns of DEGs along pseudotime in well- versus poorly differentiated groups. (G) IHC of CRABP2 in well- and poorly differentiated HNSCC tissue samples (n=5 each). Top: representative IHC images (magnification, ×10). Bottom: quantification of stained area and intensity using Image-Pro Plus software. (H) Western blot (left) and RT-PCR (right) showing expression of CRABP2 and differentiation markers (CD44, IVL) following CRABP2 knockdown in FADU cells. (I) Representative images (left) and quantification (right) of cell sphere formation in NC and siCRABP2-treated cells (magnification, ×20). *, P<0.05; **, P<0.01; ***, P<0.001. AOD, average optical density; ; DEGs, differentially expressed genes; HNSCC, head and neck squamous cell carcinoma; IHC, immunohistochemistry; NC, negative control; RT-PCR, reverse transcription polymerase chain reaction; UMAP, Uniform Manifold Approximation and Projection.

    Article Snippet: Fadu cells were obtained from the American Type Culture Collection (ATCC) and were cultured for no more than 15 passages.

    Techniques: Biomarker Discovery, Expressing, Staining, Software, Western Blot, Reverse Transcription Polymerase Chain Reaction, Knockdown, Immunohistochemistry, Negative Control, Reverse Transcription, Polymerase Chain Reaction