Expression profiles of p53/p73, NME and GLI families in metastatic melanoma tissue and cell lines
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Updated: Jan 20, 2026
Experimental Metastatic Melanoma Mouse Model: A Platform to Study the Metastatic Potential of Melanoma Cells in the Lungs
Published on: April 30, 2023
Petar Ozretić1, Nikolina Hanžić1, Bastien Proust1
1Division of Molecular Medicine, Ruđer Bošković Institute, Bijenička cesta 54, HR-10000, Zagreb, Croatia.
Abstract:
Unlike other tumours, TP53 is rarely mutated in melanoma; however, it fails to function as a tumour suppressor. We assume that its functions might be altered through interactions with several families of proteins, including p53/p73, NME and GLI. To elucidate the potential interplay among these families we analysed the expression profiles of aforementioned genes and proteins in a panel of melanoma cell lines, metastatic melanoma specimens and healthy corresponding tissue. Using qPCR a higher level of NME1 gene expression and lower levels of Δ40p53β, ΔNp73, GLI1, GLI2 and PTCH1 were observed in tumour samples compared to healthy tissue. Protein expression of Δ133p53α, Δ160p53α and ΔNp73α isoforms, NME1 and NME2, and N'ΔGLI1, GLI1FL, GLI2ΔN isoforms was elevated in tumour tissue, whereas ∆Np73β was downregulated. The results in melanoma cell lines, in general, support these findings. In addition, we correlated expression profiles with clinical features and outcome. Higher Δ133p53β and p53α mRNA and both GLI1 mRNA and GLI3R protein expression had a negative impact on the overall survival. Shorter overall survival was also connected with lower p53β and NME1 gene expression levels. In conclusion, all examined genes may have implications in melanoma development and functional inactivity of TP53.
Insights
TP53 is not often mutated in melanoma but doesn't suppress tumors. Gene expression analysis revealed altered protein interactions in melanoma, impacting patient survival.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- TP53 mutations are rare in melanoma, yet it fails as a tumor suppressor.
- TP53's tumor-suppressive function may be altered via interactions with p53/p73, NME, and GLI protein families.
Purpose of the Study:
- To investigate the interplay among p53/p73, NME, and GLI protein families in melanoma.
- To analyze gene and protein expression profiles in melanoma cell lines, metastatic tissues, and healthy controls.
Main Methods:
- Quantitative Polymerase Chain Reaction (qPCR) for gene expression analysis.
- Protein expression analysis using Western blotting or similar techniques.
- Correlation of expression profiles with clinical features and patient survival outcomes.
Main Results:
- Tumor samples showed higher NME1 gene expression and lower expression of Δ40p53β, ΔNp73, GLI1, GLI2, and PTCH1 compared to healthy tissue.
- Elevated protein levels of Δ133p53α, Δ160p53α, ΔNp73α, NME1, NME2, N'ΔGLI1, GLI1FL, and GLI2ΔN were observed in tumor tissue, with downregulation of ∆Np73β.
- Higher expression of Δ133p53β, p53α mRNA, GLI1 mRNA, and GLI3R protein correlated with negative overall survival.
Conclusions:
- The examined genes (p53/p73, NME, GLI families) play significant roles in melanoma development.
- Altered expression patterns of these proteins contribute to the functional inactivity of TP53 in melanoma.
- Specific gene expression profiles are linked to reduced overall survival in melanoma patients.
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