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Cells
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Advances in Cellular and Molecular Research in Melanoma
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Advances in Cellular and Molecular Research in Melanoma

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 21289

Special Issue Editors

Dr. Barbara Stecca

E-Mail Website
Guest Editor
Tumor Cell Biology Unit, Core Research Laboratory,Istituto per lo Studio la Prevenzione e la Rete Oncologica (ISPRO), Florence, Italy
Interests: Melanoma; Hedgehog signaling; small molecule inhibitors; stemness; metastasis
Dr. Laura Poliseno

E-Mail Website
Guest Editor
Oncogenomics Unit, Institute of Clinical Physiology (IFC), National Research Council (CNR), and Core Research Laboratory (CRL), Istituto per lo Studio, la Prevenzione e la Rete Oncologica (ISPRO), 56124 Pisa, Italy
Interests: melanoma; BRAFV600E isoforms; microRNAs; ceRNAs; pigmentation; melanoma modeling in zebrafish and mice; attenuated Listeria monocytogenes; pseudogenes
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Malignant melanoma is the most aggressive form of skin cancer and its incidence is increasing worldwide. Genetic alterations contributing to melanoma pathogenesis have been extensively studied; these include mutations in BRAF and NRAS oncogenes, as well as in a handful of tumor suppressors, such as NF1, PTEN and CDKN2A. Aberrant activation of oncogenic BRAF has provided the basis for efficient targeted therapy with specific inhibitors of mutant BRAF and MEK, although side effects are heavy and long-term clinical benefits are hampered by the development of acquired resistance. Conversely, immune checkpoint inhibitors blocking CTLA-4 or PD-1/PD-L1 have shown durable responses, although response rate still remains low.

This Special Issue aims to explore new molecular and cellular aspects associated with melanoma development, progression and treatment, including mechanisms of signal transduction, role of aberrant glycosylation and role of non-coding RNAs. It also aims at exploring the potential of such aspects as targets for novel therapeutic interventions, as well as biomarkers for screening, predicting treatment response and monitoring disease progression.   

With this Special Issue we hope to provide basic and translational researchers with an overview of breakthroughs on the molecular and cellular mechanisms/pathways involved in this dismal disease.

Dr. Barbara Stecca
Dr. Laura Poliseno
Guest Editors

Manuscript Submission Information

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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. Cells 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 2700 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

  • Mechanisms and molecular aspects associated with melanoma onset, progression, metastasis and resistance to therapy, with particular emphasis on: signal transduction; glycosylation; non-coding functions of transcripts
  • Novel molecular-based therapeutic strategies
  • Novel delivery strategies
  • Novel prognostic/predictive biomarkers

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Published Papers (6 papers)

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Research

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20 pages, 3177 KiB  
Article
MAGOH and MAGOHB Knockdown in Melanoma Cells Decreases Nonsense-Mediated Decay Activity and Promotes Apoptosis via Upregulation of GADD45A
by Agnes Soederberg, Tina Meißgeier, Anja Katrin Bosserhoff and Lisa Linck-Paulus
Cells 2022, 11(23), 3859; https://doi.org/10.3390/cells11233859 - 30 Nov 2022
Cited by 4 | Viewed by 2012
Abstract
Cutaneous malignant melanoma is a highly proliferative and aggressive skin cancer with a steadily increasing incidence and a low long-term survival rate after metastatic progression. The protein MAGOH and its highly identical homologue MAGOHB are core components of the exon junction complex (EJC), [...] Read more.
Cutaneous malignant melanoma is a highly proliferative and aggressive skin cancer with a steadily increasing incidence and a low long-term survival rate after metastatic progression. The protein MAGOH and its highly identical homologue MAGOHB are core components of the exon junction complex (EJC), which regulates splicing, stability and translation of mRNAs. The EJC, and especially MAGOH, has been shown to be involved in the development and progression of several cancers. In melanoma, the expression and function of both homologues remain essentially unexplored. This study identifies high MAGOH and MAGOHB protein expression in cutaneous melanoma cell lines and patient derived tissue samples. An siRNA-mediated knockdown of MAGOH significantly inhibits melanoma cell proliferation. The loss of MAGOH does not affect cell cycle progression, but induces apoptosis, an effect that is enhanced by a simultaneous knockdown of MAGOH and MAGOHB. MAGOH and MAGOHB do not influence the expression of the pro-apoptotic protein Bcl-XS or exon skipping. However, the knockdown of MAGOH and MAGOHB strongly decreases nonsense-mediated decay (NMD) activity, leading to an upregulation of the pro-apoptotic protein GADD45A. In conclusion, simultaneous inhibition of MAGOH and MAGOHB expression substantially affects cell survival, indicating both MAGOH homologues as promising new targets for the treatment of melanoma. Full article
(This article belongs to the Special Issue Advances in Cellular and Molecular Research in Melanoma)
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22 pages, 5790 KiB  
Article
Knockdown of Lamin B1 and the Corresponding Lamin B Receptor Leads to Changes in Heterochromatin State and Senescence Induction in Malignant Melanoma
by Lisa Lämmerhirt, Melanie Kappelmann-Fenzl, Stefan Fischer, Michaela Pommer, Tom Zimmermann, Viola Kluge, Alexander Matthies, Silke Kuphal and Anja Katrin Bosserhoff
Cells 2022, 11(14), 2154; https://doi.org/10.3390/cells11142154 - 8 Jul 2022
Cited by 13 | Viewed by 3251
Abstract
Modifications in nuclear structures of cells are implicated in several diseases including cancer. They result in changes in nuclear activity, structural dynamics and cell signalling. However, the role of the nuclear lamina and related proteins in malignant melanoma is still unknown. Its molecular [...] Read more.
Modifications in nuclear structures of cells are implicated in several diseases including cancer. They result in changes in nuclear activity, structural dynamics and cell signalling. However, the role of the nuclear lamina and related proteins in malignant melanoma is still unknown. Its molecular characterisation might lead to a deeper understanding and the development of new therapy approaches. In this study, we analysed the functional effects of dysregulated nuclear lamin B1 (LMNB1) and its nuclear receptor (LBR). According to their cellular localisation and function, we revealed that these genes are crucially involved in nuclear processes like chromatin organisation. RNA sequencing and differential gene expression analysis after knockdown of LMNB1 and LBR revealed their implication in important cellular processes driving ER stress leading to senescence and changes in chromatin state, which were also experimentally validated. We determined that melanoma cells need both molecules independently to prevent senescence. Hence, downregulation of both molecules in a BRAFV600E melanocytic senescence model as well as in etoposide-treated melanoma cells indicates both as potential senescence markers in melanoma. Our findings suggest that LMNB1 and LBR influence senescence and affect nuclear processes like chromatin condensation and thus are functionally relevant for melanoma progression. Full article
(This article belongs to the Special Issue Advances in Cellular and Molecular Research in Melanoma)
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17 pages, 1600 KiB  
Article
Comprehensive Gene Expression Analysis to Identify Differences and Similarities between Sex- and Stage-Stratified Melanoma Samples
by Eirini Chrysanthou, Emir Sehovic, Paola Ostano and Giovanna Chiorino
Cells 2022, 11(7), 1099; https://doi.org/10.3390/cells11071099 - 24 Mar 2022
Cited by 3 | Viewed by 2220
Abstract
Overall lower incidence and better prognosis are observed in female melanoma patients compared to males. As sex and stage differences in the context of melanoma gene expression are understudied, we aim to highlight them through statistical analysis of melanoma gene expression datasets. Data [...] Read more.
Overall lower incidence and better prognosis are observed in female melanoma patients compared to males. As sex and stage differences in the context of melanoma gene expression are understudied, we aim to highlight them through statistical analysis of melanoma gene expression datasets. Data from seven online datasets, including normal skin, commonly acquired nevi, and melanomas, were collected and analyzed. Sex/stage-related differences were assessed using statistical analyses on survival, gene expression, and its variability. Significantly better overall survival in females was observed in stage I, II but not in stage III. Gene expression variability was significantly different between stages and sexes. Specifically, we observed a significantly lower variability in genes expressed in normal skin and nevi in females compared to males, as well as in female stage I, II melanomas. However, in stage III, variability was lower in males. Similarly, class comparison showed that the gene expression differences between sexes are most notable in non-melanoma followed by early-stage-melanoma samples. Sexual dimorphism is an important aspect to consider for a holistic understanding of early-stage melanomas, not only from the tumor characteristics but also from the gene expression points of view. Full article
(This article belongs to the Special Issue Advances in Cellular and Molecular Research in Melanoma)
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13 pages, 1807 KiB  
Article
Prognostic Roles of BRAF, KIT, NRAS, IGF2R and SF3B1 Mutations in Mucosal Melanomas
by Joanna P. Wróblewska, Dora Dias-Santagata, Adam Ustaszewski, Cheng-Lin Wu, Masakazu Fujimoto, M. Angelica Selim, Wojciech Biernat, Janusz Ryś, Andrzej Marszalek and Mai P. Hoang
Cells 2021, 10(9), 2216; https://doi.org/10.3390/cells10092216 - 27 Aug 2021
Cited by 15 | Viewed by 2931
Abstract
Background: The prognostic value of commonly recurrent mutations remains unclear in mucosal melanomas. Methods: Clinicopathologic parameters of 214 cases of mucosal melanomas diagnosed in 1989–2020 in several clinical institutions were analyzed. NRAS, KIT, BRAF, IGF2R and SF3B1 mutational analyses by [...] Read more.
Background: The prognostic value of commonly recurrent mutations remains unclear in mucosal melanomas. Methods: Clinicopathologic parameters of 214 cases of mucosal melanomas diagnosed in 1989–2020 in several clinical institutions were analyzed. NRAS, KIT, BRAF, IGF2R and SF3B1 mutational analyses by Sanger sequencing and next generation sequencing-based assay were performed in a subset of cases. Results: Of the triple (BRAF, NRAS, NF1)-negative cases, APC, KIT and KRAS are detected mainly in sinonasal, vulvovaginal and anorectal melanomas, respectively. NRAS, KIT, BRAF, IGF2R and SF3B1 mutations are detected in 19% (37/198), 22% (44/197), 12% (25/201), 16% (22/138) and 15% (20/133) of cases, respectively. In univariate analyses, advanced stage (p = 0.016), 65 years or older (p = 0.048) and presence of ulceration (p = 0.027) are significantly correlated with worse overall survival (OS), respectively. NRAS mutation significantly correlates with worse OS (p = 0.028) and worse melanoma-specific survival (MSS) (p = 0.03) for all cases of mucosal melanomas. In multivariate analyses, NRAS mutation remains as an independent predictor of worse OS (p = 0.036) and worse MSS (p = 0.024). Conclusion: NRAS mutation is a predictor of worse survival, independent of stage in mucosal melanomas. The significance of frequently mutated IGF2R in mucosal melanomas remains unclear. Full article
(This article belongs to the Special Issue Advances in Cellular and Molecular Research in Melanoma)
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Review

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27 pages, 2901 KiB  
Review
Mitochondrial Metabolism in Melanoma
by Christina Huang, Rakan H. Radi and Jack L. Arbiser
Cells 2021, 10(11), 3197; https://doi.org/10.3390/cells10113197 - 16 Nov 2021
Cited by 17 | Viewed by 4857
Abstract
Melanoma and its associated alterations in cellular pathways have been growing areas of interest in research, especially as specific biological pathways are being elucidated. Some of these alterations include changes in the mitochondrial metabolism in melanoma. Many mitochondrial metabolic changes lead to differences [...] Read more.
Melanoma and its associated alterations in cellular pathways have been growing areas of interest in research, especially as specific biological pathways are being elucidated. Some of these alterations include changes in the mitochondrial metabolism in melanoma. Many mitochondrial metabolic changes lead to differences in the survivability of cancer cells and confer resistance to targeted therapies. While extensive work has gone into characterizing mechanisms of resistance, the role of mitochondrial adaptation as a mode of resistance is not completely understood. In this review, we wish to explore mitochondrial metabolism in melanoma and how it impacts modes of resistance. There are several genes that play a major role in melanoma mitochondrial metabolism which require a full understanding to optimally target melanoma. These include BRAF, CRAF, SOX2, MCL1, TRAP1, RHOA, SRF, SIRT3, PTEN, and AKT1. We will be discussing the role of these genes in melanoma in greater detail. An enhanced understanding of mitochondrial metabolism and these modes of resistance may result in novel combinatorial and sequential therapies that may lead to greater therapeutic benefit. Full article
(This article belongs to the Special Issue Advances in Cellular and Molecular Research in Melanoma)
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17 pages, 771 KiB  
Review
The Role of Glycosylation in Melanoma Progression
by Chiara De Vellis, Silvia Pietrobono and Barbara Stecca
Cells 2021, 10(8), 2136; https://doi.org/10.3390/cells10082136 - 19 Aug 2021
Cited by 26 | Viewed by 4895
Abstract
Malignant melanoma is the most aggressive form of skin cancer, which originates from the malignant transformation of melanocytes, the melanin-producing cells of the skin. Melanoma progression is typically described as a stepwise process in which metastasis formation ensues late during disease. A large [...] Read more.
Malignant melanoma is the most aggressive form of skin cancer, which originates from the malignant transformation of melanocytes, the melanin-producing cells of the skin. Melanoma progression is typically described as a stepwise process in which metastasis formation ensues late during disease. A large body of evidence has shown that the accumulation of genetic and epigenetic alterations drives melanoma progression through the different steps. Mortality in melanoma is associated with metastatic disease. Accordingly, early-stage melanoma can be cured in the majority of cases by surgical excision, while late-stage melanoma is a highly lethal disease. Glycosylation is a post-translational modification that involves the transfer of glycosyl moieties to specific amino acid residues of proteins to form glycosidic bonds through the activity of glycosyltransferases. Aberrant glycosylation is considered a hallmark of cancer as it occurs in the majority of tumor types, including melanoma. The most widely occurring glycosylation changes in melanoma are represented by sialylation, fucosylation, and N- and I-glycan branching. In this review, we discuss the role of glycosylation in melanoma and provide insights on the mechanisms by which aberrant glycosylation promotes melanoma progression through activation of invasion and metastasis, immune evasion and cell proliferation. Full article
(This article belongs to the Special Issue Advances in Cellular and Molecular Research in Melanoma)
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