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Melanoma: Molecular Mechanism and New Agents for Prevention and Therapy
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Melanoma: Molecular Mechanism and New Agents for Prevention and Therapy

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 20 February 2026 | Viewed by 1416

Special Issue Editor

Dr. M. Letizia Motti

E-Mail Website
Guest Editor
Department of Medical, Human Movement and Well-being Sciences, University of Naples Parthenope, 38, 80133 Napoli NA, Italy
Interests: melanoma; drug resistance melanoma; melanoma cells migration; melanoma cells invasion, apoptosis; melanoma epigenetics; cell cycle; signal transduction

Special Issue Information

Dear Colleagues,

Malignant melanoma is the most aggressive epithelial tumor with a high capacity to metastasize to various organs. Although available treatments for metastatic melanoma have significantly improved the clinical outcome of patients, there is still too large a portion of patients whose tumor progresses. This is due to the high plasticity of melanoma cells and their complex interaction with the tumor microenvironment, which can strongly influence their behavior, regulating tumor progression, and their response to therapies, leading to the development of resistance mechanisms. Therefore, new therapeutic approaches for melanoma are needed. This Special Issue aims to collect studies on the molecular mechanisms underlying melanomagenesis and tumor progression, on the identification of new targets and/or potential predictive or prognostic markers, as well as on the use of new molecules, including natural substances, for therapy. Original experimental research, review articles, and commentaries are considered.

Dr. M. Letizia Motti
Guest Editor

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Keywords

  • melanoma
  • therapy resistance
  • melanoma microenvironment (MME)
  • melanoma plasticity
  • epigenetic mechanism
  • predictive markers
  • prognostic markers
  • extracellular vesicles
  • molecular therapy
  • natural molecules

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Published Papers (2 papers)

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Research

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28 pages, 7900 KB  
Article
Sublethal Doxorubicin Promotes Extracellular Vesicle Biogenesis in A375 Melanoma Cells: Implications for Vesicle-Loaded TGF-β-Mediated Cancer Progression and Cardiovascular Pathophysiology
by Laura Fernanda Fernández-Fonseca, Susana Novoa-Herrán, Adriana Umaña-Pérez and Luis Alberto Gómez-Grosso
Int. J. Mol. Sci. 2025, 26(17), 8524; https://doi.org/10.3390/ijms26178524 - 2 Sep 2025
Viewed by 292
Abstract
Doxorubicin (Dox) is not a first-line treatment for melanoma due to limited antitumor efficacy and dose-dependent cardiotoxicity. However, sublethal doses may trigger adaptive cellular responses that influence tumor progression and systemic toxicity. Small extracellular vesicles (EVs) are key mediators of intercellular communication and [...] Read more.
Doxorubicin (Dox) is not a first-line treatment for melanoma due to limited antitumor efficacy and dose-dependent cardiotoxicity. However, sublethal doses may trigger adaptive cellular responses that influence tumor progression and systemic toxicity. Small extracellular vesicles (EVs) are key mediators of intercellular communication and can carry bioactive molecules that modulate both the tumor microenvironment and distant tissues. This study investigates how sublethal Dox exposure alters EV biogenesis and cargo in A375 melanoma cells and explores the potential implications for cardiovascular function. We treated human A375 melanoma cells with 10 nM dox for 96 h. EVs were isolated using differential ultracentrifugation and size exclusion chromatography. Vesicle characterization included Immunocytochemistry for CD63, CD81, CD9, Rab7 and TSG101, scanning electron microscopy (SEM) Nanoparticle Tracking Analysis (NTA), and Western blotting for CD81 and CytC. We analyzed cytokine content using cytokine membrane arrays. Guinea pig cardiomyocytes were exposed to the isolated vesicles, and mitochondrial activity was evaluated using the MTT assay. Statistical analysis included t-tests, ANOVA, Cohen’s d, and R2 and η2. Dox exposure significantly increased EV production (13.6-fold; p = 0.000014) and shifted vesicle size distribution. CD81 expression was significantly upregulated (p = 0.0083), and SEM (microscopy) confirmed enhanced vesiculation. EVs from treated cells were enriched in TGF-β (p = 0.0134), VEGF, CXCL1, CXCL12, CCL5, IL-3, IL-4, IL-10, Galectin-3, and KITLG. Cardiomyocytes exposed to these vesicles showed a 2.3-fold reduction in mitochondrial activity (p = 0.0021), an effect absent when vesicles were removed. Bioinformatic analysis linked EV cargo to pathways involved in cardiac hypertrophy, inflammation, and fibrosis. As conclusion, sublethal Doxorubicin reprograms melanoma-derived EVs by enhancing their production and enriching their cargo with profibrotic and immunomodulatory mediators. These vesicles may contribute to tumor progression and cardiovascular physiopathology, suggesting that targeting EVs could improve therapeutic outcomes in cancer and cardiovascular disease. Full article
(This article belongs to the Special Issue Melanoma: Molecular Mechanism and New Agents for Prevention and Therapy)
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Review

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17 pages, 513 KB  
Review
The Role of Fibroblasts in Melanoma Development: From Tumor Microenvironment Remodeling to Pre-Metastatic Niche Formation
by Immacolata Belviso, Raffaele Pastore, Aldo Mileo, Emiliano Del Genio, Stefania Boccia, Stefano Palermi, Carmine Sellitto and Maria Letizia Motti
Int. J. Mol. Sci. 2025, 26(13), 6132; https://doi.org/10.3390/ijms26136132 - 26 Jun 2025
Viewed by 859
Abstract
Melanoma is the most aggressive form of skin cancer, and despite significant therapeutic advances over the past decade, a substantial number of patients still progress to a fatal outcome. The initiation and progression of melanoma are strongly influenced by interactions between melanoma cells [...] Read more.
Melanoma is the most aggressive form of skin cancer, and despite significant therapeutic advances over the past decade, a substantial number of patients still progress to a fatal outcome. The initiation and progression of melanoma are strongly influenced by interactions between melanoma cells and other components of the tumor microenvironment (TME). In this review, we focus on the interplay between fibroblasts resident in the tumor microenvironment and tumor cells. In particular, we examine the molecular mechanisms through which melanoma cells induce the transformation of resident fibroblasts into their active form, known as cancer-associated fibroblasts (CAFs). We also explore the role of CAFs in shaping the melanoma microenvironment (MME) and in organizing the pre-metastatic niche, a specialized microenvironment that forms in distant organs or tissues to support the survival and expansion of metastatic melanoma cells. Finally, we discuss emerging therapeutic strategies aimed at disrupting the interactions between CAFs, melanoma cells, and other components of the tumor microenvironment to improve treatment outcomes. Full article
(This article belongs to the Special Issue Melanoma: Molecular Mechanism and New Agents for Prevention and Therapy)
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