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Cancers
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Mechanisms of Melanoma Progression
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Mechanisms of Melanoma Progression

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: 1 May 2024 | Viewed by 3979

Special Issue Editor

Dr. Mohamed Hassan

E-Mail Website
Guest Editor
1. Research Laboratory of Surgery-Oncology, Department of Surgery, Tulane University School of Medicine, New Orleans, LA 70112, USA
2. Institut National de la Santé et de la Recherche Médicale, S1121, University of Strasbourg, 67000 Strasbourg, France
Interests: cancer research; melanoma research; cancer stem-like cells; tumor progression; metastasis and recurrence; molecular tumor therapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Melanoma progression, metastasis and drug resistance are not only driven by irreversible genetic instability, but also by reversible and functional reprograming of signaling routes. PI3K, together with downstream dependent and/or converged routes, is able to mediate extra- or intra-transduction signals, leading to the initiation of tumor development, progression and resistance. In a wide spectrum of human cancers, the function of tumor-growth-driving signals in tumor progression and metastasis has gained more attention over the years, while the function of tumor-resistance-driving signals is under-investigated. The activation of PI3K has been established as a direct consequence of the inactivation of the tumor suppressor protein PTEN (phosphatase and tensin homolog deleted on chromosome 10), activation of receptors tyrosine kinases, amplification of Akt family members or mutations of PI3K subunits; however, its activation in a CSCs-dependent manner is poorly described. Signaling through the Ras/Raf/MEK/ERK and Ras/PI3K/PTEN/Akt/mTOR pathways is tightly regulated and mainly starts from the cell surface to initiate a controlled gene expression within the nucleus. This course of regulation is mediated by a series of kinases, phosphatases and various exchange proteins. Genetic and epigenetic alteration of the key components of these pathways can mediate uncontrolled mechanisms, leading to the generation of aberrant signaling routes. The extraordinary activation of aberrant signals, such as the PI3K pathway in a CSCs-dependent manner, may have significant consequences on melanoma progression, metastasis, treatment resistance and recurrence.

The aim of this Special Issue is to update the current findings addressing the role of receptor and non-receptor tyrosine kinases in melanoma progression and treatment resistance.

Dr. Mohamed Hassan
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • melanoma progression
  • metastasis
  • drug resistance
  • signaling pathway

Published Papers (3 papers)

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Research

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18 pages, 2609 KiB  
Article
Cancer Cell Biomechanical Properties Accompany Tspan8-Dependent Cutaneous Melanoma Invasion
by Gaël Runel, Noémie Lopez-Ramirez, Laetitia Barbollat-Boutrand, Muriel Cario, Simon Durand, Maxime Grimont, Manfred Schartl, Stéphane Dalle, Julie Caramel, Julien Chlasta and Ingrid Masse
Cancers 2024, 16(4), 694; https://doi.org/10.3390/cancers16040694 - 06 Feb 2024
Viewed by 1149
Abstract
The intrinsic biomechanical properties of cancer cells remain poorly understood. To decipher whether cell stiffness modulation could increase melanoma cells’ invasive capacity, we performed both in vitro and in vivo experiments exploring cell stiffness by atomic force microscopy (AFM). We correlated stiffness properties [...] Read more.
The intrinsic biomechanical properties of cancer cells remain poorly understood. To decipher whether cell stiffness modulation could increase melanoma cells’ invasive capacity, we performed both in vitro and in vivo experiments exploring cell stiffness by atomic force microscopy (AFM). We correlated stiffness properties with cell morphology adaptation and the molecular mechanisms underlying epithelial-to-mesenchymal (EMT)-like phenotype switching. We found that melanoma cell stiffness reduction was systematically associated with the acquisition of invasive properties in cutaneous melanoma cell lines, human skin reconstructs, and Medaka fish developing spontaneous MAP-kinase-induced melanomas. We observed a systematic correlation of stiffness modulation with cell morphological changes towards mesenchymal characteristic gains. We accordingly found that inducing melanoma EMT switching by overexpressing the ZEB1 transcription factor, a major regulator of melanoma cell plasticity, was sufficient to decrease cell stiffness and transcriptionally induce tetraspanin-8-mediated dermal invasion. Moreover, ZEB1 expression correlated with Tspan8 expression in patient melanoma lesions. Our data suggest that intrinsic cell stiffness could be a highly relevant marker for human cutaneous melanoma development. Full article
(This article belongs to the Special Issue Mechanisms of Melanoma Progression)
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Review

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26 pages, 1640 KiB  
Review
Mechanisms of Melanoma Progression and Treatment Resistance: Role of Cancer Stem-like Cells
by Youssef Al Hmada, Robert T. Brodell, Naji Kharouf, Thomas W. Flanagan, Abdulhadi A. Alamodi, Sofie-Yasmin Hassan, Hosam Shalaby, Sarah-Lilly Hassan, Youssef Haikel, Mosaad Megahed, Simeon Santourlidis and Mohamed Hassan
Cancers 2024, 16(2), 470; https://doi.org/10.3390/cancers16020470 - 22 Jan 2024
Viewed by 1522
Abstract
Melanoma is the third most common type of skin cancer, characterized by its heterogeneity and propensity to metastasize to distant organs. Melanoma is a heterogeneous tumor, composed of genetically divergent subpopulations, including a small fraction of melanoma-initiating cancer stem-like cells (CSCs) and many [...] Read more.
Melanoma is the third most common type of skin cancer, characterized by its heterogeneity and propensity to metastasize to distant organs. Melanoma is a heterogeneous tumor, composed of genetically divergent subpopulations, including a small fraction of melanoma-initiating cancer stem-like cells (CSCs) and many non-cancer stem cells (non-CSCs). CSCs are characterized by their unique surface proteins associated with aberrant signaling pathways with a causal or consequential relationship with tumor progression, drug resistance, and recurrence. Melanomas also harbor significant alterations in functional genes (BRAF, CDKN2A, NRAS, TP53, and NF1). Of these, the most common are the BRAF and NRAS oncogenes, with 50% of melanomas demonstrating the BRAF mutation (BRAFV600E). While the successful targeting of BRAFV600E does improve overall survival, the long-term efficacy of available therapeutic options is limited due to adverse side effects and reduced clinical efficacy. Additionally, drug resistance develops rapidly via mechanisms involving fast feedback re-activation of MAPK signaling pathways. This article updates information relevant to the mechanisms of melanoma progression and resistance and particularly the mechanistic role of CSCs in melanoma progression, drug resistance, and recurrence. Full article
(This article belongs to the Special Issue Mechanisms of Melanoma Progression)
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13 pages, 1544 KiB  
Review
Melanin—The Éminence Grise of Melanoma and Parkinson’s Disease Development
by Danuta Krasowska, Agata Małek, Joanna Kurzepa, Lucyna Kapka-Skrzypczak, Dorota Krasowska and Jacek Kurzepa
Cancers 2023, 15(23), 5541; https://doi.org/10.3390/cancers15235541 - 23 Nov 2023
Viewed by 1018
Abstract
A common feature of Parkinson’s disease (PD) and melanoma is their starting points being based on cells capable of converting tyrosine into melanin. Melanocytes produce two types of melanin: eumelanin and pheomelanin. These dyes are designed to protect epidermal cells from the harmful [...] Read more.
A common feature of Parkinson’s disease (PD) and melanoma is their starting points being based on cells capable of converting tyrosine into melanin. Melanocytes produce two types of melanin: eumelanin and pheomelanin. These dyes are designed to protect epidermal cells from the harmful effects of UV radiation. Neurones of the substantia nigra, which degenerate during PD, produce neuromelanin, the physiological role of which is not fully explained. This article discusses the potential role of melanins in the pathogenesis of both diseases. Melanins, due to their ability to accumulate toxic substances, may become their sources over time. The use of glutathione for the synthesis of pheomelanins and neuromelanins may reduce the antioxidant capacity of cells, leading to an excessive synthesis of free radicals. This study also tested the hypothesis that certain drugs used in the treatment of PD (L-DOPA, MAO-B and COMT inhibitors, and amantadine), aimed at increasing dopamine concentration, could potentially contribute to the development of melanoma. The role and properties of melanins should continue to be researched. Whether excessive melanin synthesis or its accumulation in the extracellular space may be factors initiating the development of diseases remains an open question. Full article
(This article belongs to the Special Issue Mechanisms of Melanoma Progression)
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