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: Frontiers in Oncology

Article Title: Downregulation of HDGF inhibits tumorigenic phenotypes of hypopharyngeal squamous cell carcinoma by suppressing the AKT/mTOR/VEGF pathway

doi: 10.3389/fonc.2025.1683145

Figure Lengend Snippet: Expression characteristics and functional enrichment of HDGF in hypopharyngeal squamous cell carcinoma (HSCC). (A) HDGF expression was significantly higher in HSCC tissues than in normal tissues ( P < 0.001). (B) Paired analysis confirmed HDGF upregulation in tumors compared with matched normal samples ( P < 0.001). (C) HDGF expression increased with histologic grade and was highest in G3 tumors ( P < 0.001). (D) HDGF levels elevated with clinical stage and were higher in stage IV than stage I ( P < 0.05). (E) HDGF expression was higher in male patients. (G) HDGF levels were elevated in patients with lymphovascular invasion ( P < 0.05). (H) Patients with a history of radiotherapy showed higher HDGF expression ( P < 0.05). (I) GO Molecular Function analysis revealed enrichment in telomeric DNA binding and telomerase RNA binding. (J) GO Biological Process terms included telomere maintenance, telomere organization, and regulation of chromosomal organization. (K) GO Cellular Component terms included chromosomal region, centromeric region, kinetochore, condensed chromosome, and telomerase holoenzyme complex. (L) Heatmap of differentially expressed genes (DEGs) between normal and HSCC tissues. Data are presented as mean ± SD. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Article Snippet: The human FaDu HSCC cell line was obtained from the American Type Cell Collection (ATCC; Manassas, VA, USA).

Techniques: Expressing, Functional Assay, Binding Assay, RNA Binding Assay

Journal: Frontiers in Oncology

Article Title: Downregulation of HDGF inhibits tumorigenic phenotypes of hypopharyngeal squamous cell carcinoma by suppressing the AKT/mTOR/VEGF pathway

doi: 10.3389/fonc.2025.1683145

Figure Lengend Snippet: Effects of HDGF knockdown on proliferation and colony formation of FaDu cells. (A) Lentiviral transduction efficiency (>80% GFP-positive cells; magnification, ×200). (B) Relative HDGF mRNA expression in FaDu cells after transduction. (C) HDGF protein expression in FaDu cells after transduction. (D) CCK-8 assay showing reduced proliferation of FaDu cells after HDGF knockdown. (E, F) Colony formation assay demonstrating reduced colony formation capacity after HDGF knockdown. Data are mean ± SD; * P < 0.05, ** P < 0.01, *** P < 0.001,**** P < 0.0001.

Article Snippet: The human FaDu HSCC cell line was obtained from the American Type Cell Collection (ATCC; Manassas, VA, USA).

Techniques: Knockdown, Transduction, Expressing, CCK-8 Assay, Colony Assay

Journal: Frontiers in Oncology

Article Title: Downregulation of HDGF inhibits tumorigenic phenotypes of hypopharyngeal squamous cell carcinoma by suppressing the AKT/mTOR/VEGF pathway

doi: 10.3389/fonc.2025.1683145

Figure Lengend Snippet: Effects of HDGF depletion on migration and invasion of FaDu cells. (A, B) Wound healing assay (representative images at x100 magnification). (C, D) Transwell migration assay (representative images at x100 magnification). (E, F) Transwell Matrigel invasion assay (representative images at x100 magnification). HDGF knockdown significantly reduced migration (A-D) and invasion (E, F) capacities. Data are mean ± SD; * P < 0.05, ** P < 0.01, *** P < 0.001,**** P < 0.0001.

Article Snippet: The human FaDu HSCC cell line was obtained from the American Type Cell Collection (ATCC; Manassas, VA, USA).

Techniques: Migration, Wound Healing Assay, Transwell Migration Assay, Invasion Assay, Knockdown

Journal: Frontiers in Oncology

Article Title: Downregulation of HDGF inhibits tumorigenic phenotypes of hypopharyngeal squamous cell carcinoma by suppressing the AKT/mTOR/VEGF pathway

doi: 10.3389/fonc.2025.1683145

Figure Lengend Snippet: Effects of HDGF knockdown on EMT and AKT/mTOR/VEGF signaling in FaDu cells. (A, B) Western blot analysis of EMT-related proteins: N-cadherin, Snail, and Slug decreased; E-cadherin increased after HDGF knockdown. (C, D) Western blot analysis of AKT/mTOR/VEGF pathway components: p-AKT, p-mTOR, and VEGFA decreased after HDGF knockdown. Data are mean ± SD; * P < 0.05, ** P < 0.01, *** P < 0.001,**** P < 0.0001.

Article Snippet: The human FaDu HSCC cell line was obtained from the American Type Cell Collection (ATCC; Manassas, VA, USA).

Techniques: Knockdown, Western Blot