Expression of LOXL3, NES, and SNAI1 in Melanoma Genesis and Progression

Author:

Šitum Čeprnja Zdenka1,Kelam Nela2ORCID,Ogorevc Marin2ORCID,Racetin Anita2,Vukoja Martina3,Čeprnja Toni4,Filipović Natalija2ORCID,Saraga-Babić Mirna2,Vukojević Katarina25ORCID

Affiliation:

1. Department of Dermatovenerology, University Hospital of Split, 21000 Split, Croatia

2. Department of Anatomy, Histology and Embryology, University of Split School of Medicine, 21000 Split, Croatia

3. Laboratory of Morphology, Department of Histology and Embryology, School of Medicine, University of Mostar, 88 000 Mostar, Bosnia and Herzegovina

4. Department of Pathology, Forensic Medicine and Cytology, University Hospital of Split, 21000 Split, Croatia

5. Center for Translational Research in Biomedicine, University of Split School of Medicine, 21000 Split, Croatia

Abstract

Melanoma is the most severe type of skin cancer and among the most malignant neoplasms in humans. With the growing incidence of melanoma, increased numbers of therapeutic options, and the potential to target specific proteins, understanding the basic mechanisms underlying the disease’s progression and resistance to treatment has never been more important. LOXL3, SNAI1, and NES are key factors in melanoma genesis, regulating tumor growth, metastasis, and cellular differentiation. In our study, we explored the potential role of LOXL3, SNAI1, and NES in melanoma progression and metastasis among patients with dysplastic nevi, melanoma in situ, and BRAF+ and BRAF− metastatic melanoma, using immunofluorescence and qPCR analysis. Our results reveal a significant increase in LOXL3 expression and the highest NES expression in BRAF+ melanoma compared to BRAF−, dysplastic nevi, and melanoma in situ. As for SNAI1, the highest expression was observed in the metastatic melanoma group, without significant differences among groups. We found co-expression of LOXL3 and SNAI1 in the perinuclear area of all investigated subgroups and NES and SNAI1 co-expression in melanoma cells. These findings suggest a codependence or collaboration between these markers in melanoma EMT, suggesting new potential therapeutic interventions to block the EMT cascade that could significantly affect survival in many melanoma patients.

Funder

Croatian Science Foundation

Publisher

MDPI AG

Reference48 articles.

1. Heistein, J.B., Acharya, U., and Mukkamalla, S.K.R. (2024). Malignant Melanoma. StatPearls [Internet], StatPearls Publishing.

2. Melanoma Epidemic: An Analysis of Six Decades of Data From the Connecticut Tumor Registry;Geller;J. Clin. Oncol.,2013

3. European consensus-based interdisciplinary guideline for melanoma. Part 1: Diagnostics: Update 2022;Garbe;Eur. J. Cancer,2022

4. Melanoma: Epidemiology, risk factors, pathogenesis, diagnosis and classification;Rastrelli;In Vivo,2014

5. The Genetic Evolution of Melanoma from Precursor Lesions;Shain;N. Engl. J. Med.,2015

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