neck cancer cell lines fadu  (ATCC)

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

Journal: International Journal of Biological Sciences

Article Title: Oncogenic RARγ isoforms promote head and neck cancer proliferation through vinexin-β-mediated cell cycle acceleration and autocrine activation of EGFR signal

doi: 10.7150/ijbs.100351

Figure Lengend Snippet: Expression of RARγ isoforms in head and neck cancer (HNC) tissues and various cell lines. (a) Schematic illustration showing the cDNA structure of the five RARγ isoforms. Arrows indicate primer pairs designed to detect the expression of each RARγ isoform. (b) The mRNA expression of RARγ isoforms in HOK (primary human normal oral keratinocytes), SG (immortalized human oral keratinocytes), DOK (dysplstic human oral keratinocytes) and various HNC cell lines (FaDu, HSC3, OC3, OECM1, SAS). (c) Representative RT-PCR results of RARγ isoform detection in oral squamous carcinomas (OSCC) (T) and their corresponding adjacent non-tumor epithelia (N). (d) The relative abundance of each RARγ isoform in the 20 pairs of OSCC (T) and their adjacent non-tumor epithelia (N). (e) Confocal microscopic study to reveal the localization of RARγ1, RARγ2, flag-tagged RARγ4 and all RARγs in HNC cells (RARγ1, RARγ4-flag and all RARγs in red fluorescence; RARγ2 in green fluorescence; Nuclei were stained blue with DAPI). Scale bar: 10 μm. (f) Representative immunohistochemical (IHC) study conducted on expression and localization of RAR γ 1, RAR γ 2 in normal epithelia (upper panel), adjacent non-tumor epithelia of oral squamous cell carcinoma (OSCC) (middle panel), and OSCC tumors (lower panel). Scale bar: 100 μm (upper and middle panel); 50 μm (lower panel) (g) Expression patterns of RARγ isoforms in various types of human cancer, and immortalized non-cancer cell lines (MCF10A, Z183A, and Z172).

Article Snippet: Figure b demonstrates the expression patterns of the five RARγ isoforms in normal human oral keratinocytes (HOK), immortalized oral keratinocytes (SG), dysplastic oral keratinocytes (DOK), and head and neck cancer cell lines (FaDu, HSC3, OC3, OECM1, SAS).

Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction, Fluorescence, Staining, Immunohistochemical staining

Journal: International Journal of Biological Sciences

Article Title: Oncogenic RARγ isoforms promote head and neck cancer proliferation through vinexin-β-mediated cell cycle acceleration and autocrine activation of EGFR signal

doi: 10.7150/ijbs.100351

Figure Lengend Snippet: Role of RARγ isoforms in growth-modulation of HNC cells. (a) Proliferation assays showing the growth-modulation effects of RAR γ isoforms in SG, DOK, FaDu, SAS and OC3 cells. (b) Schematic illustration showing the protein structures of RAR γ 1, 2, 4, 5. Four distinct domain structures are noted in RAR γ , including an AF-1 domain, a DNA-bindin domain (DBD), a ligand-binding domain (LBD), and a C-terminal AF-2 domain. The AF-1 domain of RAR γ 1, 2, 4 contains a proline-rich area with two phospho-regulatory serine residues. Another phospho-regulatory serine residue is located at the LBD (Ser 299 of RAR γ 4). (c) Phospho-defective Ser 7 (RARγ4-S7A) suppressed RAR γ 4-mediated growth-promotion of FaDu and SAS cells. (d) The effect of phospho-mimic Ser 7 (RAR γ 4-S7E) on HNC cell proliferation. (e) The phosphorylation status of Ser 299 did not impact RAR γ 4-mediated proliferation of FaDu and SAS cells. (f) RAR γ 4-enhanced HNC proliferation is RA-dependent. Mutation of the RA-binding pocket (RAR γ 4-R324G) significantly impaired RA binding and attenuated RAR γ 4-mediated growth promotion in FaDu and SAS cells. (g) Nude mice inoculated subcutaneously with SAS-RAR γ 4, SAS-RAR γ 4-S7A, SAS-RAR γ 4-R324G, or vector control (n = 8). Tumor volumes were measured twice a week. *p < 0.05; **p < 0.01; ***p < 0.001.

Article Snippet: Figure b demonstrates the expression patterns of the five RARγ isoforms in normal human oral keratinocytes (HOK), immortalized oral keratinocytes (SG), dysplastic oral keratinocytes (DOK), and head and neck cancer cell lines (FaDu, HSC3, OC3, OECM1, SAS).

Techniques: Ligand Binding Assay, Residue, Mutagenesis, Binding Assay, Plasmid Preparation, Control

Journal: Cell Death & Disease

Article Title: Genomic and transcriptomic profiling of radioresistant prostate and head and neck cancers implicate a BAHD1-dependent modification of DNA damage at the heterochromatin

doi: 10.1038/s41419-024-07316-y

Figure Lengend Snippet: A Differentially expressed genes (DEGs) in 22Rv1 and DU145, and ( B ) in FaDu and DU145. The DEGs were defined if the adjusted P < 0.05. C Expression profile of 221 common DEGs with consistent dysregulation direction in both 22Rv1 and DU145. D Expression profile of 1420 common DEGs with consistent dysregulation direction in both FaDu and HK1. Samples were ordered by cell lines and phenotype in both figures. E 18 DEGs with consistent dysregulation direction across four cell lines. The colour of each dot indicates the dysregulation direction, with red indicating upregulation and blue indicating downregulation. The size of each dot varies based on its fold change. The intensity of colour within each box reflects the range of P -values. F Significant pathways involved by the 5 upregulated DEGs across the 4 cell lines, curated from over-representation analysis (false discovery rate <0.1). The colour intensity within each colour filled box represents the rich factor of the gene in the pathway.

Article Snippet: Prostate and head and neck cancer cell lines 22Rv1, DU145, and FaDu were purchased from the American Type Culture Collection (ATCC), routinely tested for mycoplasma contamination with EZ-PCT TM Mycoplasma Detection Kit (Biological Industries, USA) and authenticated using short tandem repeat analysis by ATCC (ATCC, USA).

Techniques: Expressing

Journal: Cell Death & Disease

Article Title: Genomic and transcriptomic profiling of radioresistant prostate and head and neck cancers implicate a BAHD1-dependent modification of DNA damage at the heterochromatin

doi: 10.1038/s41419-024-07316-y

Figure Lengend Snippet: A The representative western blot showed the changes in the expression of DSB, DNA repair, cell cycle arrest and heterochromatin markers under different time points post-4 Gy IR (normalised against control), GAPDH was used as a loading control. B and C-top panel Representative images of H3K9me3 (green) and H3K27me3 (red) foci in 22Rv1 cells at 0 and 1 h treatment time points and FaDu cells at 0 and 6 h treatment time points. Scale bar: 5 μm. B and C-bottom panel H3K9me3 intensity was quantified in AUCs and represented as percentage frequencies, compared between RR and WT; H3K27me3 foci were quantified as mean foci per cell, bars represent mean±SD, n = 3 per group. DSB DNA double-strand break, AUC area under the curve, WT wild-type, SD standard deviation.

Article Snippet: Prostate and head and neck cancer cell lines 22Rv1, DU145, and FaDu were purchased from the American Type Culture Collection (ATCC), routinely tested for mycoplasma contamination with EZ-PCT TM Mycoplasma Detection Kit (Biological Industries, USA) and authenticated using short tandem repeat analysis by ATCC (ATCC, USA).

Techniques: Western Blot, Expressing, Control, Standard Deviation

Journal: Cell Death & Disease

Article Title: Genomic and transcriptomic profiling of radioresistant prostate and head and neck cancers implicate a BAHD1-dependent modification of DNA damage at the heterochromatin

doi: 10.1038/s41419-024-07316-y

Figure Lengend Snippet: A and B-top left Representative images of H3K9me3 (green) and H3K27me3 (red) foci in 22Rv1 cells at 1 h and FaDu cells at 6 h post-siBAHD1 treatment. Scale bar: 5 μm; (top right) Representative western blot showed the changes in H3K9me3 and H3K27me3 protein levels in 22Rv1 cells at 1 h and FaDu cells at 6 h post-siBAHD1 treatment; (bottom panel) H3K9me3 intensity was quantified in AUCs and represented as percentage frequencies, compared between RR and WT; H3K27me3 foci were quantified as mean foci per cell, bars represent mean±SD, n = 3 per group. C Colony forming assay of 22Rv1 and FaDu cells under different IR dosages, with and without siBAHD1 treatment, n = 3 per group. Asterisk indicates significance between siBAHD1-treated and control groups. Asterisk indicates P < 0.05.

Article Snippet: Prostate and head and neck cancer cell lines 22Rv1, DU145, and FaDu were purchased from the American Type Culture Collection (ATCC), routinely tested for mycoplasma contamination with EZ-PCT TM Mycoplasma Detection Kit (Biological Industries, USA) and authenticated using short tandem repeat analysis by ATCC (ATCC, USA).

Techniques: Western Blot, Control

Journal: Cell Death & Disease

Article Title: Genomic and transcriptomic profiling of radioresistant prostate and head and neck cancers implicate a BAHD1-dependent modification of DNA damage at the heterochromatin

doi: 10.1038/s41419-024-07316-y

Figure Lengend Snippet: A A hypothesised model showing BAHD1 contributes to the enhanced heterochromatin response in RR cancer cells, whereby increased repair efficiency following irradiation (IR)-induced damage leads to decreased radiosensitivity. The inhibition of BAHD1 leads to chromatin unpacking, decreased repair efficiency and improved radiosensitivity (created with Biorender.com). B and C, left Representative images of co-localised γH2AX (green) and p-53BP1 (red) foci in 22Rv1-RR and FaDu-RR cells at 1 and 6 h post-IR, with and without siBAHD1 treatment. Scale bar: 5 μm; ( right ) Quantification of co-localised γH2AX and p-53BP1 mean foci per cell, bars represent mean±SD, n = 3 per group. D, E Representative western blot showed the changes in the expression of DSB, DNA repair, cell cycle arrest and heterochromatin markers of 22Rv1-RR cells and FaDu-RR cells at 1 and 6 h post-IR, with and without siBAHD1 treatment (normalised against control).

Article Snippet: Prostate and head and neck cancer cell lines 22Rv1, DU145, and FaDu were purchased from the American Type Culture Collection (ATCC), routinely tested for mycoplasma contamination with EZ-PCT TM Mycoplasma Detection Kit (Biological Industries, USA) and authenticated using short tandem repeat analysis by ATCC (ATCC, USA).

Techniques: Irradiation, Inhibition, Western Blot, Expressing, Control