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Cells
Special Issues
Melanoma: From Molecular Mechanisms to Therapeutic Opportunities—Series 2
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Melanoma: From Molecular Mechanisms to Therapeutic Opportunities—Series 2

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

Deadline for manuscript submissions: 20 December 2024 | Viewed by 4218

Special Issue Editors

Prof. Dr. Cynthia Simbulan-Rosenthal

E-Mail Website
Guest Editor
Department of Biochemistry and Molecular & Cellular Biology, Georgetown University School of Medicine, Washington, DC, USA
Interests: apoptosis; genotoxicity; skin biology; melanoma; cancer; cell proliferation
Special Issues, Collections and Topics in MDPI journals
Dr. Dean S. Rosenthal

E-Mail Website
Guest Editor
Department of Biochemistry and Molecular & Cellular Biology, Georgetown University School of Medicine, Washington, DC, USA
Interests: apoptosis; genotoxicity; DNA damage; skin biology; wound healing; melanoma; cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to announce the second edition of our Special Issue. The first edition attracted the interest of researchers around the world. The publications that are freely available for download are listed at the following:

Cells website: https://www.mdpi.com/journal/cells/special_issues/Melanoma_Molecular_Mechanism

Malignant melanoma remains a formidable challenge, with ~106,110 new cases and ~7,180 deaths in the United States in 2021. Drug and immune resistance, together with invasion and metastasis, determine tumor progression, and, ultimately, patient survival. With the highest mortality rate among skin cancers, cutaneous melanoma is associated with driver mutations in MAPK and other signaling pathways, including RAS/PI3K/AKT, p16INK4a/CDK4/RB, WNT, and p53. Activating mutations are primarily in the V600 or K601 of BRAF (50% of melanomas), Q61 of NRAS (>20%), and LOF mutations in NF1 (10%). Although combinations of targeted kinase inhibitors for BRAF and MEK, combined with immune checkpoint inhibitors, have improved progression-free and overall survival of melanoma patients, ~75% of melanomas recur after BRAF copy number gains, alternative splicing, MEK1/2, and NRAS gain-of-function mutations; 20% of BRAFi-resistant melanomas upregulate compensatory PI3K/AKT survival pathways. Although treatment for recalcitrant NRAS-mutant metastatic tumors has advanced, with immunotherapies anti–PD-1, anti-PD-L1, and/or anti-CTLA4 proving efficacious, many patients remain unresponsive, and chemotherapy with dacarbazine, temozolomide, or carboplatin shows limited success.  There is a compelling rationale to examine unexploited pathways. Resistance has been attributed to subpopulations of “melanoma initiating cells”, highly tumorigenic cancer stem cells characterized by melanosphere formation, and expression of specific cancer stem cell markers.

This Special Issue will publish original articles and reviews focusing on novel targets for therapeutic intervention; biomarkers for screening, predicting treatment response, and monitoring disease progression; and mechanistic insights and advances in molecular and cellular pathways involved in melanomagenesis and progression. Topics of interest include mechanisms underlying melanoma progression and treatment response, signal transduction, melanoma-initiating cells, drug resistance, invasiveness, immune evasion, and metastasis. There remains an urgent need to identify novel targets and develop new combinatorial therapeutic approaches that can overcome drug resistance mechanisms.

We look forward to receiving your contributions to this Special Issue.

Prof. Dr. Cynthia Simbulan-Rosenthal
Dr. Dean S. Rosenthal
Guest Editors

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. 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

  • melanomagenesis
  • treatment response
  • signal transduction
  • melanoma initiating cells
  • drug resistance
  • invasiveness
  • immune evasion
  • metastasis
  • MAPK pathway
  • PI3K/AKT survival pathways
  • MEKi
  • BRAFi
  • trametinib
  • dabrafenib
  • immunotherapies

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Published Papers (3 papers)

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Research

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17 pages, 3224 KiB  
Article
Impact of Nannochloropsis oceanica and Chlorococcum amblystomatis Extracts on UVA-Irradiated on 3D Cultured Melanoma Cells: A Proteomic Insight
by Agnieszka Gęgotek, Tiago Conde, Maria Rosário Domingues, Pedro Domingues and Elżbieta Skrzydlewska
Cells 2024, 13(23), 1934; https://doi.org/10.3390/cells13231934 - 21 Nov 2024
Viewed by 245
Abstract
Melanoma is one of the most malignant forms of skin cancer, characterised by the highest mortality rate among affected patients. This study aims to analyse and compare the effects of lipid extracts from the microalgae Nannochloropsis oceanica (N.o.) and Chlorococcum amblystomatis [...] Read more.
Melanoma is one of the most malignant forms of skin cancer, characterised by the highest mortality rate among affected patients. This study aims to analyse and compare the effects of lipid extracts from the microalgae Nannochloropsis oceanica (N.o.) and Chlorococcum amblystomatis (C.a.) on the intra and extracellular proteome of UVA-irradiated melanoma cells using a three-dimensional model. Proteomic analysis revealed that UVA radiation significantly increases the levels of pro-inflammatory proteins in melanoma cells. Treatment with algae extracts reduced these protein levels in both non-irradiated and irradiated cells. Furthermore, untreated cells released proteins responsible for cell growth and proliferation into the medium, a process hindered by UVA radiation through the promotion of pro-inflammatory molecules secretion. The treatment with algae extracts effectively mitigated UVA-induced alterations. Notably, UVA radiation significantly induced the formation of 4-HNE and 15-PGJ2 protein adducts in both cells and the medium, while treatment with algae extracts stimulated the formation of 4-HNE-protein adducts and reduced the level of 15-PGJ2-protein adducts. However, both algae extracts successfully prevented these UVA-induced modifications. In conclusion, lipid extracts from N.o. and C.a. appear to be promising agents in supporting anti-melanoma therapy. However, their potent protective capacity may limit their applicability, particularly following cells exposure to UVA. Full article
(This article belongs to the Special Issue Melanoma: From Molecular Mechanisms to Therapeutic Opportunities—Series 2)
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21 pages, 13417 KiB  
Article
CD133 Stimulates Cell Proliferation via the Upregulation of Amphiregulin in Melanoma
by Cynthia M Simbulan-Rosenthal, Nusrat Islam, Yogameenakshi Haribabu, Ryyan Alobaidi, Azadeh Shalamzari, Garrett Graham, Li-Wei Kuo, Peter Sykora and Dean S Rosenthal
Cells 2024, 13(9), 777; https://doi.org/10.3390/cells13090777 - 2 May 2024
Cited by 1 | Viewed by 1917
Abstract
CD133, a cancer stem cell (CSC) marker in tumors, including melanoma, is associated with tumor recurrence, chemoresistance, and metastasis. Patient-derived melanoma cell lines were transduced with a Tet-on vector expressing CD133, generating doxycycline (Dox)-inducible cell lines. Cells were exposed to Dox for 24 [...] Read more.
CD133, a cancer stem cell (CSC) marker in tumors, including melanoma, is associated with tumor recurrence, chemoresistance, and metastasis. Patient-derived melanoma cell lines were transduced with a Tet-on vector expressing CD133, generating doxycycline (Dox)-inducible cell lines. Cells were exposed to Dox for 24 h to induce CD133 expression, followed by RNA-seq and bioinformatic analyses, revealing genes and pathways that are significantly up- or downregulated by CD133. The most significantly upregulated gene after CD133 was amphiregulin (AREG), validated by qRT-PCR and immunoblot analyses. Induced CD133 expression significantly increased cell growth, percentage of cells in S-phase, BrdU incorporation into nascent DNA, and PCNA levels, indicating that CD133 stimulates cell proliferation. CD133 induction also activated EGFR and the MAPK pathway. Potential mechanisms highlighting the role(s) of CD133 and AREG in melanoma CSC were further delineated using AREG/EGFR inhibitors or siRNA knockdown of AREG mRNA. Treatment with the EGFR inhibitor gefitinib blocked CD133-induced cell growth increase and MAPK pathway activation. Importantly, siRNA knockdown of AREG reversed the stimulatory effects of CD133 on cell growth, indicating that AREG mediates the effects of CD133 on cell proliferation, thus serving as an attractive target for novel combinatorial therapeutics in melanoma and cancers with overexpression of both CD133 and AREG. Full article
(This article belongs to the Special Issue Melanoma: From Molecular Mechanisms to Therapeutic Opportunities—Series 2)
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Review

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14 pages, 291 KiB  
Review
Role of Surgery in Metastatic Melanoma and Review of Melanoma Molecular Characteristics
by Kulkaew Sukniam, Harsheen K. Manaise, Kyle Popp, Reed Popp and Emmanuel Gabriel
Cells 2024, 13(6), 465; https://doi.org/10.3390/cells13060465 - 7 Mar 2024
Cited by 4 | Viewed by 1591
Abstract
We aimed to review the molecular characteristics of metastatic melanoma and the role of surgery in metastasectomy for metastatic melanoma. We performed a systematic literature search on PubMed to identify relevant studies focusing on several mutations, including NRAS, BRAF, NF1, MITF, PTEN, TP53, [...] Read more.
We aimed to review the molecular characteristics of metastatic melanoma and the role of surgery in metastasectomy for metastatic melanoma. We performed a systematic literature search on PubMed to identify relevant studies focusing on several mutations, including NRAS, BRAF, NF1, MITF, PTEN, TP53, CDKN2A, TERT, TMB, EGFR, and c-KIT. This was performed in the context of metastatic melanoma and the role of metastasectomy in the metastatic melanoma population. A comprehensive review of these molecular characteristics is presented with a focus on their prognosis and role in surgical metastasectomy. Full article
(This article belongs to the Special Issue Melanoma: From Molecular Mechanisms to Therapeutic Opportunities—Series 2)
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