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Special Issue "Molecular and Cellular Mechanisms of Cancers: Cutaneous Melanoma"

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

Deadline for manuscript submissions: closed (30 November 2020) | Viewed by 15507

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Prof. Dr. Massimo Libra

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Department of Biomedical and Biotechnological Sciences, Universita degli Studi di Catania, 95123 Catania, Italy
Interests: general pathology; oncology; cancer development; drug resistance; epigenetics
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Dr. Luca Falzone

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Department of Biomedical and Biotechnological Sciences, Universita degli Studi di Catania, Catania, Italy
Interests: cancer; epigenetics; biomarkers; microRNAs; DNA methylation; occupational carcinogens
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Dear Colleagues,

Cutaneous melanoma (CM) represents one of the most aggressive types of cancer because of its high metastatic power. Several environmental risk factors have been recognized for the development of CM, as well as different molecular mechanisms responsible for the malignant transformation of melanocytes. Notably, the alteration of the RAS/RAF/MEK/ERK and PI3K/AKT/mTOR signal transduction pathways are key mechanisms involved in the development of CM, but a growing body of evidence has demonstrated that epigenetic alterations and tumor microenvironment modifications may promote melanoma development and progression. These findings have led to the development of new targeted therapies that ameliorate the overall survival of melanoma patients; however, the mortality rate of CM still remains high due to the development of drug resistance mechanisms.

Therefore, the identification of the molecular mechanisms responsible for therapeutic failure is one of the main goals for the treatment of cutaneous melanomas. Furthermore, the study of epigenetic alterations and tumor microenvironment modifications in patients with melanoma could provide useful information to identify new therapeutic targets and find new early diagnostic and prognostic biomarkers for CM.

On these bases, the focus of this Special Issue will be the evaluation of the molecular and cellular mechanisms involved in melanoma development, progression, aggressiveness, and drug resistance in order to provide updated information about the current status of molecular, pharmaceutical and translational scientific discoveries in the field of Cutaneous Melanoma.

Potential topics will include but are not limited to:

Environmental and occupational risk factors for cutaneous melanoma;
Epigenetics modifications and cutaneous melanoma development and progression;
Novel biomarkers for the early diagnosis of cutaneous melanoma;
Molecular alterations associated with cutaneous melanoma;
Tumor microenvironment and matrix metalloproteinases in cutaneous melanoma: Roles and clinical implications;
Therapeutic strategies for cutaneous melanoma;
Natural compounds as novel therapeutic strategies;
Molecular mechanisms and strategies to overcome drug resistance in cutaneous melanoma.

We look forward to your contributions.

Prof. Massimo Libra
Dr. Luca Falzone
Guest Editors

Manuscript Submission Information

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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

cutaneous melanoma
immunotherapy
targeted therapy
drug resistance
RAF and PI3K pathways

Published Papers (4 papers)

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Research

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16 pages, 2351 KiB

Open AccessArticle

A Potential Role of RUNX2- RUNT Domain in Modulating the Expression of Genes Involved in Bone Metastases: An In Vitro Study with Melanoma Cells

Maria Grazia Romanelli

Monica Mottes

Donato Zipeto

and

Maria Teresa Valenti

Cells 2020, 9(3), 751; https://doi.org/10.3390/cells9030751 - 19 Mar 2020

Cited by 6 | Viewed by 2995

Abstract

Ectopic expression of RUNX2 has been reported in several tumors. In melanoma cells, the RUNT domain of RUNX2 increases cell proliferation and migration. Due to the strong link between RUNX2 and skeletal development, we hypothesized that the RUNT domain may be involved in the modulation of mechanisms associated with melanoma bone metastasis. Therefore, we evaluated the expression of metastatic targets in wild type (WT) and RUNT KO melanoma cells by array and real-time PCR analyses. Western blot, ELISA, immunofluorescence, migration and invasion ability assays were also performed. Our findings showed that the expression levels of bone sialoprotein (BSP) and osteopontin (SPP1) genes, which are involved in malignancy-induced hypercalcemia, were reduced in RUNT KO cells. In addition, released PTHrP levels were lower in RUNT KO cells than in WT cells. The RUNT domain also contributes to increased osteotropism and bone invasion in melanoma cells. Importantly, we found that the ERK/p-ERK and AKT/p-AKT pathways are involved in RUNT-promoted bone metastases. On the basis of our findings, we concluded that the RUNX2 RUNT domain is involved in the mechanisms promoting bone metastasis of melanoma cells via complex interactions between multiple players involved in bone remodeling. Full article

(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Cancers: Cutaneous Melanoma)

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28 pages, 4302 KiB

Open AccessArticle

Dissecting Mechanisms of Melanoma Resistance to BRAF and MEK Inhibitors Revealed Genetic and Non-Genetic Patient- and Drug-Specific Alterations and Remarkable Phenotypic Plasticity

Mariusz L. Hartman

Malgorzata Sztiller-Sikorska

Anna Gajos-Michniewicz

and

Malgorzata Czyz

Cells 2020, 9(1), 142; https://doi.org/10.3390/cells9010142 - 07 Jan 2020

Cited by 36 | Viewed by 4151

Abstract

The clinical benefit of MAPK pathway inhibition in BRAF-mutant melanoma patients is limited by the development of acquired resistance. Using drug-naïve cell lines derived from tumor specimens, we established a preclinical model of melanoma resistance to vemurafenib or trametinib to provide insight into resistance mechanisms. Dissecting the mechanisms accompanying the development of resistance, we have shown that (i) most of genetic and non-genetic alterations are triggered in a cell line- and/or drug-specific manner; (ii) several changes previously assigned to the development of resistance are induced as the immediate response to the extent measurable at the bulk levels; (iii) reprogramming observed in cross-resistance experiments and growth factor-dependence restricted by the drug presence indicate that phenotypic plasticity of melanoma cells largely contributes to the sustained resistance. Whole-exome sequencing revealed novel genetic alterations, including a frameshift variant of RBMX found exclusively in phospho-AKT^high resistant cell lines. There was no similar pattern of phenotypic alterations among eleven resistant cell lines, including expression/activity of crucial regulators, such as MITF, AXL, SOX, and NGFR, which suggests that patient-to-patient variability is richer and more nuanced than previously described. This diversity should be considered during the development of new strategies to circumvent the acquired resistance to targeted therapies. Full article

(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Cancers: Cutaneous Melanoma)

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21 pages, 5654 KiB

Open AccessArticle

Dibutyltin(IV) and Tributyltin(IV) Derivatives of meso-Tetra(4-sulfonatophenyl)porphine Inhibit the Growth and the Migration of Human Melanoma Cells

and

Cells 2019, 8(12), 1547; https://doi.org/10.3390/cells8121547 - 30 Nov 2019

Cited by 4 | Viewed by 2382

Abstract

Melanoma is the most aggressive and deadly form of skin cancer, which is largely due to its propensity to metastasize. Therefore, with the aim to inhibit the growth and the metastatic dissemination of melanoma cells and to provide a novel treatment option, we studied the effects of the melanoma treatment with two organotin(IV) complexes of the meso-tetra(4-sulfonato-phenyl)porphine, namely (Bu₂Sn)₂TPPS and (Bu₃Sn)₄TPPS. In particular, we showed that nanomolar concentrations of (Bu₂Sn)₂TPPS and (Bu₃Sn)₄TPPS are sufficient to inhibit melanoma cell growth, to increase the expression of the full-length poly (ADP-ribose) polymerase (PARP-1), to induce the cell cycle arrest respectively at G2/M and G0/G1 through the inhibition of the Cyclin D1 expression and to inhibit cell colony formation. Nanomolar concentrations of (Bu₂Sn)₂TPPS and (Bu₃Sn)₄TPPS are also sufficient to inhibit the melanoma cell migration and the expression of some adhesion receptors. Moreover, we report that (Bu₂Sn)₂TPPS and (Bu₃Sn)₄TPPS act downstream of BRAF, mainly bypassing its functions, but targeting the STAT3 signalling protein. Finally, these results suggest that (Bu₂Sn)₂TPPS and (Bu₃Sn)₄TPPS may be effective therapeutic strategies for their role in the inhibition of melanoma growth and migration. Full article

(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Cancers: Cutaneous Melanoma)

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36 pages, 2699 KiB

Open AccessReview

Human Plasmacytoid Dendritic Cells and Cutaneous Melanoma

and

Cells 2020, 9(2), 417; https://doi.org/10.3390/cells9020417 - 11 Feb 2020

Cited by 21 | Viewed by 5322

Abstract

The prognosis of metastatic melanoma (MM) patients has remained poor for a long time. However, the recent introduction of effective target therapies (BRAF and MEK inhibitors for BRAFV600-mutated MM) and immunotherapies (anti-CTLA-4 and anti-PD-1) has significantly improved the survival of MM patients. Notably, all these responses are highly dependent on the fitness of the host immune system, including the innate compartment. Among immune cells involved in cancer immunity, properly activated plasmacytoid dendritic cells (pDCs) exert an important role, bridging the innate and adaptive immune responses and directly eliminating cancer cells. A distinctive feature of pDCs is the production of high amount of type I Interferon (I-IFN), through the Toll-like receptor (TLR) 7 and 9 signaling pathway activation. However, published data indicate that melanoma-associated escape mechanisms are in place to hijack pDC functions. We have recently reported that pDC recruitment is recurrent in the early phases of melanoma, but the entire pDC compartment collapses over melanoma progression. Here, we summarize recent advances on pDC biology and function within the context of melanoma immunity. Full article

(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Cancers: Cutaneous Melanoma)

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Special Issue "Molecular and Cellular Mechanisms of Cancers: Cutaneous Melanoma"

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