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Melanoma: From Molecular Pathology to Therapeutic Approaches
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Melanoma: From Molecular Pathology to Therapeutic Approaches

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 April 2024) | Viewed by 5596

Special Issue Editor

Prof. Dr. Michael Eccles

E-Mail Website
Guest Editor
Department of Pathology, Dunedin School of Medicine, University of Otago, Dunedin 9016, New Zealand
Interests: genomics; epigenomics; melanomas; human cancer; PAX genes; transcriptomic
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

While melanoma is one of the most aggressive and devastating cancer types, major advances in both melanoma targeted therapy as well as immunotherapy over the past two decades have revolutionised melanoma treatment. These advances have been driven by technical innovation aimed at targeting molecular pathological biomarkers, which facilitate melanoma cell killing.

However, despite these therapeutic advances, a significant proportion of melanoma patients still do not benefit from these treatments, which is due to either innate or acquired treatment resistance in the melanomas.

In this Special Issue, we welcome authors to submit original research and review articles which contribute to a better understanding of molecular pathological biomarkers and mechanisms leading to treatment resistance in melanoma. Topics of interest include, but are not limited to:

  • Intrinsic therapeutic resistance mechanisms, immune pathways or tumour microenvironmental factors affecting cutaneous, mucosal, uveal or other melanoma types.
  • Novel small molecules or environmental factors affecting treatment resistance, or therapeutic response in melanoma.
  • Individual ‘omics or integrated ‘omics studies of molecular (nucleotide variant, gene expression, or epigenetic) mechanisms involved in melanoma treatment response.
  • Relationships between gene expression and epigenetic mechanisms of therapeutic response in melanoma.
  • New therapeutic strategies (including combination therapeutic approaches) targeting melanoma tissues.

Prof. Dr. Michael Eccles
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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.

Published Papers (5 papers)

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Research

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19 pages, 6380 KiB  
Article
Quercetin Impairs the Growth of Uveal Melanoma Cells by Interfering with Glucose Uptake and Metabolism
by Aysegül Tura, Viktoria Herfs, Tjorge Maaßen, Huaxin Zuo, Siranush Vardanyan, Michelle Prasuhn, Mahdy Ranjbar, Vinodh Kakkassery and Salvatore Grisanti
Int. J. Mol. Sci. 2024, 25(8), 4292; https://doi.org/10.3390/ijms25084292 - 12 Apr 2024
Viewed by 429
Abstract
Monosomy 3 in uveal melanoma (UM) increases the risk of lethal metastases, mainly in the liver, which serves as the major site for the storage of excessive glucose and the metabolization of the dietary flavonoid quercetin. Although primary UMs with monosomy 3 exhibit [...] Read more.
Monosomy 3 in uveal melanoma (UM) increases the risk of lethal metastases, mainly in the liver, which serves as the major site for the storage of excessive glucose and the metabolization of the dietary flavonoid quercetin. Although primary UMs with monosomy 3 exhibit a higher potential for basal glucose uptake, it remains unknown as to whether glycolytic capacity is altered in such tumors. Herein, we initially analyzed the expression of n = 151 genes involved in glycolysis and its interconnected branch, the “pentose phosphate pathway (PPP)”, in the UM cohort of The Cancer Genome Atlas Study and validated the differentially expressed genes in two independent cohorts. We also evaluated the effects of quercetin on the growth, survival, and glucose metabolism of the UM cell line 92.1. The rate-limiting glycolytic enzyme PFKP was overexpressed whereas the ZBTB20 gene (locus: 3q13.31) was downregulated in the patients with metastases in all cohorts. Quercetin was able to impair proliferation, viability, glucose uptake, glycolysis, ATP synthesis, and PPP rate-limiting enzyme activity while increasing oxidative stress. UMs with monosomy 3 display a stronger potential to utilize glucose for the generation of energy and biomass. Quercetin can prevent the growth of UM cells by interfering with glucose metabolism. Full article
(This article belongs to the Special Issue Melanoma: From Molecular Pathology to Therapeutic Approaches)
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14 pages, 3758 KiB  
Article
Endothelial Mitochondria Transfer to Melanoma Induces M2-Type Macrophage Polarization and Promotes Tumor Growth by the Nrf2/HO-1-Mediated Pathway
by Fu-Chen Kuo, Hsin-Yi Tsai, Bi-Ling Cheng, Kuen-Jang Tsai, Ping-Chen Chen, Yaw-Bin Huang, Chung-Jung Liu, Deng-Chyang Wu, Meng-Chieh Wu, Bin Huang and Ming-Wei Lin
Int. J. Mol. Sci. 2024, 25(3), 1857; https://doi.org/10.3390/ijms25031857 - 03 Feb 2024
Viewed by 958
Abstract
Gynecologic tract melanoma is a malignant tumor with poor prognosis. Because of the low survival rate and the lack of a standard treatment protocol related to this condition, the investigation of the mechanisms underlying melanoma progression is crucial to achieve advancements in the [...] Read more.
Gynecologic tract melanoma is a malignant tumor with poor prognosis. Because of the low survival rate and the lack of a standard treatment protocol related to this condition, the investigation of the mechanisms underlying melanoma progression is crucial to achieve advancements in the relevant gynecological surgery and treatment. Mitochondrial transfer between adjacent cells in the tumor microenvironment regulates tumor progression. This study investigated the effects of endothelial mitochondria on the growth of melanoma cells and the activation of specific signal transduction pathways following mitochondrial transplantation. Mitochondria were isolated from endothelial cells (ECs) and transplanted into B16F10 melanoma cells, resulting in the upregulation of proteins associated with tumor growth. Furthermore, enhanced antioxidation and mitochondrial homeostasis mediated by the Sirt1-PGC-1α-Nrf2-HO-1 pathway were observed, along with the inhibition of apoptotic protein caspase-3. Finally, the transplantation of endothelial mitochondria into B16F10 cells promoted tumor growth and increased M2-type macrophages through Nrf2/HO-1-mediated pathways in a xenograft animal model. In summary, the introduction of exogenous mitochondria from ECs into melanoma cells promoted tumor growth, indicating the role of mitochondrial transfer by stromal cells in modulating a tumor’s phenotype. These results provide valuable insights into the role of mitochondrial transfer and provide potential targets for gynecological melanoma treatment. Full article
(This article belongs to the Special Issue Melanoma: From Molecular Pathology to Therapeutic Approaches)
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16 pages, 1585 KiB  
Article
Kinase Suppressor of RAS 1 (KSR1) Maintains the Transformed Phenotype of BRAFV600E Mutant Human Melanoma Cells
by Zhi Liu, Aleksandar Krstic, Ashish Neve, Cristina Casalou, Nora Rauch, Kieran Wynne, Hilary Cassidy, Amanda McCann, Emma Kavanagh, Brendan McCann, Alfonso Blanco, Jens Rauch and Walter Kolch
Int. J. Mol. Sci. 2023, 24(14), 11821; https://doi.org/10.3390/ijms241411821 - 23 Jul 2023
Viewed by 1851
Abstract
Kinase Suppressor of RAS 1 (KSR1) is a scaffolding protein for the RAS-RAF-MEK-ERK pathway, which is one of the most frequently altered pathways in human cancers. Previous results have shown that KSR1 has a critical role in mutant RAS-mediated transformation. Here, we examined [...] Read more.
Kinase Suppressor of RAS 1 (KSR1) is a scaffolding protein for the RAS-RAF-MEK-ERK pathway, which is one of the most frequently altered pathways in human cancers. Previous results have shown that KSR1 has a critical role in mutant RAS-mediated transformation. Here, we examined the role of KSR1 in mutant BRAF transformation. We used CRISPR/Cas9 to knock out KSR1 in a BRAFV600E-transformed melanoma cell line. KSR1 loss produced a complex phenotype characterised by impaired proliferation, cell cycle defects, decreased transformation, decreased invasive migration, increased cellular senescence, and increased apoptosis. To decipher this phenotype, we used a combination of proteomic ERK substrate profiling, global protein expression profiling, and biochemical validation assays. The results suggest that KSR1 directs ERK to phosphorylate substrates that have a critical role in ensuring cell survival. The results further indicate that KSR1 loss induces the activation of p38 Mitogen-Activated Protein Kinase (MAPK) and subsequent cell cycle aberrations and senescence. In summary, KSR1 function plays a key role in oncogenic BRAF transformation. Full article
(This article belongs to the Special Issue Melanoma: From Molecular Pathology to Therapeutic Approaches)
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Review

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30 pages, 1774 KiB  
Review
Development of Personalized Strategies for Precisely Battling Malignant Melanoma
by Armond J. Isaak, GeGe R. Clements, Rand Gabriel M. Buenaventura, Glenn Merlino and Yanlin Yu
Int. J. Mol. Sci. 2024, 25(9), 5023; https://doi.org/10.3390/ijms25095023 (registering DOI) - 04 May 2024
Viewed by 216
Abstract
Melanoma is the most severe and fatal form of skin cancer, resulting from multiple gene mutations with high intra-tumor and inter-tumor molecular heterogeneity. Treatment options for patients whose disease has progressed beyond the ability for surgical resection rely on currently accepted standard therapies, [...] Read more.
Melanoma is the most severe and fatal form of skin cancer, resulting from multiple gene mutations with high intra-tumor and inter-tumor molecular heterogeneity. Treatment options for patients whose disease has progressed beyond the ability for surgical resection rely on currently accepted standard therapies, notably immune checkpoint inhibitors and targeted therapies. Acquired resistance to these therapies and treatment-associated toxicity necessitate exploring novel strategies, especially those that can be personalized for specific patients and/or populations. Here, we review the current landscape and progress of standard therapies and explore what personalized oncology techniques may entail in the scope of melanoma. Our purpose is to provide an up-to-date summary of the tools at our disposal that work to circumvent the common barriers faced when battling melanoma. Full article
(This article belongs to the Special Issue Melanoma: From Molecular Pathology to Therapeutic Approaches)
18 pages, 4085 KiB  
Review
Genetic Concordance in Primary Cutaneous Melanoma and Matched Metastasis: A Systematic Review and Meta-Analysis
by Thamila Kerkour, Catherine Zhou, Loes Hollestein and Antien Mooyaart
Int. J. Mol. Sci. 2023, 24(22), 16281; https://doi.org/10.3390/ijms242216281 - 14 Nov 2023
Cited by 1 | Viewed by 1162
Abstract
Studying primary melanoma and its corresponding metastasis has twofold benefits. Firstly, to better understand tumor biology, and secondly, to determine which sample should be examined in assessing drug targets. This study systematically analyzed all the literature on primary melanoma and its matched metastasis. [...] Read more.
Studying primary melanoma and its corresponding metastasis has twofold benefits. Firstly, to better understand tumor biology, and secondly, to determine which sample should be examined in assessing drug targets. This study systematically analyzed all the literature on primary melanoma and its matched metastasis. Following PRISMA guidelines, we searched multiple medical databases for relevant publications from January 2000 to December 2022, assessed the quality of the primary-level studies using the QUIPS tool, and summarized the concordance rate of the most reported genes using the random-effects model. Finally, we evaluated the inter-study heterogeneity using the subgroup analysis. Thirty-one studies investigated the concordance of BRAF and NRAS in 1220 and 629 patients, respectively. The pooled concordance rate was 89.4% [95% CI: 84.5; 93.5] for BRAF and 97.8% [95% CI: 95.8; 99.4] for NRAS. When high-quality studies were considered, only BRAF mutation status consistency increased. Five studies reported the concordance status of c-KIT (93%, 44 patients) and TERT promoter (64%, 53 patients). Lastly, three studies analyzed the concordance of cancer genes involved in the signaling pathways, apoptosis, and proliferation, such as CDKN2A (25%, four patients), TP53 (44%, nine patients), and PIK3CA (20%, five patients). Our study found that the concordance of known drug targets (mainly BRAF) during melanoma progression is higher than in previous meta-analyses, likely due to advances in molecular techniques. Furthermore, significant heterogeneity exists in the genes involved in the melanoma genetic makeup; although our results are based on small patient samples, more research is necessary for validation. Full article
(This article belongs to the Special Issue Melanoma: From Molecular Pathology to Therapeutic Approaches)
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