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Updated: May 14, 2026

Establishment and Characterization of Patient-Derived Xenograft Models of Anaplastic Thyroid Carcinoma and Head and Neck Squamous Cell Carcinoma
Published on: June 2, 2023
Head and neck cancer cells and xenografts are very sensitive to palytoxin: decrease of c-jun n-terminale kinase-3
Tibor Görögh1, László Bèress, Elgar S Quabius
1Department of Otorhinolaryngology- Head and Neck Surgery, Section of Experimental Oncology, University of Kiel Schleswig-Holstein, Kiel, 24105, Germany. gorogh@hno.uni-kiel.de
Objectives:
Palytoxin (PTX), a marine toxin isolated from the Cnidaria (zooanthid) Palythoa caribaeorum is one of the most potent non-protein substances known. It is a very complex molecule that presents both lipophilic and hydrophilic areas. The effect of PTX was investigated in a series of experiments conducted in head and neck squamous cell carcinoma (HNSCC) cell lines and xenografts.
Materials And Methods:
Cell viability, and gene expression of the sodium/potassium-transporting ATPase subumit alpha1 (ATP1AL1) and GAPDH were analyzed in HNSCC cells and normal epithelial cells after treatment with PTX using cytotoxicity-, clonogenic-, and enzyme inhibitor assays as well as RT-PCR and Northern Blotting. For xenograft experiments severe combined immunodeficient (SCID) mice were used to analyze tumor regression. The data were statistically analyzed using One-Way Annova (SPSS vs20).
Results:
Significant toxic effects were observed in tumor cells treated with PTX (LD50 of 1.5 to 3.5 ng/ml) in contrast to normal cells. In tumor cells PTX affected both the release of LDH and the expression of the sodium/potassium-transporting ATPase subunit alpha1 gene suggesting loss of cellular integrity, primarily of the plasma membrane. Furthermore, strong repression of the c-Jun N-terminal kinase 3 (JNK3) mRNA expression was found in carcinoma cells which correlated with enhanced toxicity of PTX suggesting an essential role of the mitogen activated protein kinase (MAPK)/JNK signalling cascades pathway in the mechanisms of HNSCC cell resistance to PTX. In mice inoculated with carcinoma cells, injections of PTX into the xenografted tumors resulted within 24 days in extensive tumor destruction in 75% of the treated animals (LD50 of 68 ng/kg to 83 ng/kg) while no tumor regression occurred in control animals.
Conclusions:
These results clearly provide evidence that PTX possesses preferential toxicity for head and neck carcinoma cells and therefore it is worth further studying its impact which may extend our knowledge of the biology of head and neck cancer.
Insights
Palytoxin (PTX) demonstrates selective toxicity against head and neck squamous cell carcinoma (HNSCC) cells, offering a potential new avenue for cancer therapy. Further research into PTX
Area of Science:
- Marine biology
- Toxicology
- Oncology
Background:
- Palytoxin (PTX) is a potent marine toxin from Palythoa caribaeorum.
- PTX is a complex molecule with both lipophilic and hydrophilic properties.
- Head and neck squamous cell carcinoma (HNSCC) is a significant health concern.
Purpose of the Study:
- To investigate the effects of PTX on HNSCC cell lines and xenografts.
- To determine the selective toxicity of PTX towards cancer cells versus normal cells.
- To explore the underlying mechanisms of PTX's action in HNSCC.
Main Methods:
- Cytotoxicity, clonogenic, and enzyme inhibitor assays were used to assess cell viability.
- Gene expression analysis (RT-PCR, Northern Blotting) for ATP1AL1 and GAPDH.
- Tumor regression was analyzed in SCID mouse xenografts.
Main Results:
- PTX exhibited significant toxicity to HNSCC cells (LD50 1.5-3.5 ng/ml) but not normal cells.
- PTX affected cellular integrity and gene expression, including repression of JNK3 mRNA.
- Xenograft studies showed extensive tumor destruction in 75% of PTX-treated mice.
Conclusions:
- PTX displays preferential toxicity for HNSCC cells.
- PTX warrants further investigation for its potential in head and neck cancer treatment.
- These findings may advance the understanding of HNSCC biology and therapeutic strategies.
