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Signaling in Melanoma 2.0
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Signaling in Melanoma 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (30 November 2021) | Viewed by 5232

Special Issue Editor

Dr. Malgorzata Czyz

E-Mail Website
Guest Editor
Department of Molecular Biology of Cancer, Medical University of Lodz, 92-215 Lodz, Poland
Interests: melanoma; genome; phenotype
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Melanoma is highly heterogeneous, with cell subpopulations exerting transcriptionally distinct phenotypes. It is a consequence of diverse genetic alterations, but also of non-genomic changes often induced by the tumor microenvironment. These changes are integrated into the active modifications of multiple signaling pathways, including, but not limited to, the mitogen-activated protein kinase (MAPK) pathway and phosphoinositol-3-kinase (PI3K) pathway, which license melanoma cell survival, progression, and drug resistance. An analysis of the clinical samples derived from the melanoma patients that developed resistance to targeted therapies or immunotherapies created the opportunity to follow the changes in several critical signaling pathways.

This Special Issue of the International Journal of Molecular Sciences aims to bring together the state-of-the-art views and original research on “Signaling in Melanoma”. It will focus on the alterations in the signaling pathways that are crucial for melanoma initiation and progression, interactions of melanoma cells with the tumor microenvironment, and the development of resistance to targeted therapies and immunotherapies.

Dr. Malgorzata Czyz
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.

Keywords

  • melanoma
  • immunotherapy
  • targeted therapy
  • signaling pathways
  • tumor microenvironment

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Published Papers (2 papers)

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Research

16 pages, 3363 KiB  
Article
Relevance of BRAF Subcellular Localization and Its Interaction with KRAS and KIT Mutations in Skin Melanoma
by Marius-Alexandru Beleaua, Ioan Jung, Cornelia Braicu, Doina Milutin and Simona Gurzu
Int. J. Mol. Sci. 2021, 22(21), 11918; https://doi.org/10.3390/ijms222111918 - 3 Nov 2021
Cited by 1 | Viewed by 2099
Abstract
Although skin melanoma (SKM) represents only one-quarter of newly diagnosed skin malignant tumors, it presents a high mortality rate. Hence, new prognostic and therapeutic tools need to be developed. This study focused on investigating the prognostic value of the subcellular expression of BRAF, [...] Read more.
Although skin melanoma (SKM) represents only one-quarter of newly diagnosed skin malignant tumors, it presents a high mortality rate. Hence, new prognostic and therapeutic tools need to be developed. This study focused on investigating the prognostic value of the subcellular expression of BRAF, KRAS, and KIT in SKM in correlation with their gene-encoding interactions. In silico analysis of the abovementioned gene interactions, along with their mRNA expression, was conducted, and the results were validated at the protein level using immunohistochemical (IHC) stains. For IHC expression, the encoded protein expressions were checked on 96 consecutive SKMs and 30 nevi. The UALCAN database showed no prognostic value for the mRNA expression level of KRAS and BRAF and demonstrated a longer survival for patients with low mRNA expression of KIT in SKMs. IHC examinations of SKMs confirmed the UALCAN data and showed that KIT expression was inversely correlated with ulceration, Breslow index, mitotic rate, and pT stage. KRAS expression was also found to be inversely correlated with ulceration and perineural invasion. When the subcellular expression of BRAF protein was recorded (nuclear vs. cytoplasmatic vs. mixed nucleus + cytoplasm), a direct correlation was emphasized between nuclear positivity and lymphovascular or perineural invasion. The independent prognostic value was demonstrated for mixed expression of the BRAF protein in SKM. BRAF cytoplasmic predominance, in association with KIT’s IHC positivity, was more frequently observed in early-stage nonulcerated SKMs, which displayed a low mitotic rate and a late death event. The present study firstly verified the possible prognostic value of BRAF subcellular localization in SKMs. A low mRNA expression or IHC cytoplasmic positivity for KIT and BRAF might be used as a positive prognostic parameter of SKM. SKM’s BRAF nuclear positivity needs to be evaluated in further studies as a possible indicator of perineural and lymphovascular invasion. Full article
(This article belongs to the Special Issue Signaling in Melanoma 2.0)
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17 pages, 8204 KiB  
Article
Deciphering the Functional Role of RIPK4 in Melanoma
by Ewelina Madej, Damian Ryszawy, Anna A. Brożyna, Malgorzata Czyz, Jaroslaw Czyz and Agnieszka Wolnicka-Glubisz
Int. J. Mol. Sci. 2021, 22(21), 11504; https://doi.org/10.3390/ijms222111504 - 25 Oct 2021
Cited by 5 | Viewed by 2619
Abstract
The receptor-interacting protein kinase 4 (RIPK4) plays an important role in the development and maintenance of various tissues including skin, but its role in melanoma has not been reported. Using patient-derived cell lines and clinical samples, we show that RIPK4 is expressed in [...] Read more.
The receptor-interacting protein kinase 4 (RIPK4) plays an important role in the development and maintenance of various tissues including skin, but its role in melanoma has not been reported. Using patient-derived cell lines and clinical samples, we show that RIPK4 is expressed in melanomas at different levels. This heterogenous expression, together with very low level of RIPK4 in melanocytes, indicates that the role of this kinase in melanoma is context-dependent. While the analysis of microarray data has revealed no straightforward correlation between the stage of melanoma progression and RIPK4 expression in vivo, relatively high levels of RIPK4 are in metastatic melanoma cell lines. RIPK4 down-regulation by siRNA resulted in the attenuation of invasive potential as assessed by time-lapse video microscopy, wound-healing and transmigration assays. These effects were accompanied by reduced level of pro-invasive proteins such as MMP9, MMP2, and N-cadherin. Incubation of melanoma cells with phorbol ester (PMA) increased PKC-1β level and hyperphosphorylation of RIPK4 resulting in degradation of RIPK4. Interestingly, incubation of cells with PMA for short and long durations revealed that cell migration is controlled by the NF-κB signaling in a RIPK4-dependent (RIPK4high) or independent (RIPK4low) manner depending on cell origin (distant or lymph node metastasis) or phenotype (mesenchymal or epithelial). Full article
(This article belongs to the Special Issue Signaling in Melanoma 2.0)
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