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Cancer: Molecular Research and Novel Inflammatory Targets
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Cancer: Molecular Research and Novel Inflammatory Targets

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: 20 July 2025 | Viewed by 1862

Special Issue Editors

Dr. Sarah Adriana Scuderi

E-Mail Website
Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Viale Ferdinando Stagno D’Alcontres, 31, 98166 Messina, Italy
Interests: cancer; neuro-oncology; chemotherapy; inflammation
Special Issues, Collections and Topics in MDPI journals
Dr. Alessia Filippone

E-Mail Website
Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Messina, Italy
Interests: neuroinflammation; central nervous system; degeneration; molecular pathways; protein trafficking
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cancer is a leading cause of deaths around the world. Cancer development and its response to therapy are regulated by several factors, including inflammation, which may promote or inhibit tumor progression, exhibiting contrasting effects on therapeutic outcomes. Although there are many effective clinical treatment options, the survival rate for cancer patients is still low; thus, research on new and alternative therapeutic targets represents an important goal in the field of oncology research. Since its discovery, cancer-related inflammation has been considered a key feature of cancer, with a well-established link between chronic inflammation and tumor development. Given the relationship between inflammation and tumor, exploiting inflammation appears to be an important approach for a more efficient anti-cancer treatment.

Therefore, the aim of this Special Issue is to present new potential therapeutic targets to counteract cancer progression via inflammatory pathway modulation.

This Special Issue welcomes original research articles and reviews.

Dr. Sarah Adriana Scuderi
Dr. Alessia Filippone
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. 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

  • cancer
  • tumor microenvironment
  • molecular biology
  • biomarkers
  • novel and alternative therapies
  • inflammation
  • pharmacological inhibitors

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Published Papers (2 papers)

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17 pages, 3178 KiB  
Article
KRAS–SOS-1 Inhibition as New Pharmacological Target to Counteract Anaplastic Thyroid Carcinoma (ATC)
by Deborah Mannino, Rossella Basilotta, Fabiola De Luca, Giovanna Casili, Emanuela Esposito and Irene Paterniti
Int. J. Mol. Sci. 2025, 26(6), 2579; https://doi.org/10.3390/ijms26062579 - 13 Mar 2025
Viewed by 175
Abstract
Anaplastic thyroid carcinoma (ATC) is the most aggressive type of thyroid cancer. Tumor cells have been shown to activate alternative signaling pathways, making treatments less effective. One of the major proteins involved in the progression of ATC is the proto-oncogene KRAS that belongs [...] Read more.
Anaplastic thyroid carcinoma (ATC) is the most aggressive type of thyroid cancer. Tumor cells have been shown to activate alternative signaling pathways, making treatments less effective. One of the major proteins involved in the progression of ATC is the proto-oncogene KRAS that belongs to a group of small guanosine triphosphate (GTP)-binding proteins. Despite its recognized importance in cancer malignancy, KRAS is considered non-druggable and has never been studied in the field of ATC. In this context, a new synthetic molecule, BAY-293, has recently been developed that selectively inhibits the KRAS–SOS-1 interaction. Based on these findings, the aim of this study was to evaluate for the first time the antitumor effect of BAY-293 using in vitro and in vivo models of ATC. The in vitro model included different thyroid cancer (TC) cell lines used to study the effect of BAY-293 on the modulation of mitogen-activated protein kinase (MAPK) pathways, apoptosis, and cell migration. To confirm the in vitro findings and better mimic the complex tumor microenvironment, an in vivo orthotopic model of ATC was used. The results of the study indicate that BAY-293, both in vitro and in vivo, effectively blocked the KRAS/MAPK/ERK pathway and β-catenin, which act as downstream effectors essential for cell migration, and increased the apoptotic process by slowing the progression of ATC. In conclusion, this study demonstrated that KRAS/SOS-1 inhibition could be a promising therapeutic target for the treatment of ATC and highlighted BAY-293 as an innovative molecule that needs further research to fully evaluate its efficacy in the field of thyroid cancer. Full article
(This article belongs to the Special Issue Cancer: Molecular Research and Novel Inflammatory Targets)
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22 pages, 10687 KiB  
Article
Role of Ciminalum-4-thiazolidinone Hybrids in Molecular NF-κB Dependent Pathways
by Dominika Szlachcikowska, Anna Tabęcka-Łonczyńska, Serhii Holota, Olexandra Roman, Yulia Shepeta, Roman Lesyk and Konrad A. Szychowski
Int. J. Mol. Sci. 2024, 25(13), 7329; https://doi.org/10.3390/ijms25137329 - 3 Jul 2024
Cited by 1 | Viewed by 1246
Abstract
A range of hybrid molecules incorporating the ciminalum moiety in the thiazolidinone ring demonstrate significant anticancer and antimicrobial properties. Therefore, the aim of our study was to evaluate the properties and mechanism of action of two 4-thiazolidinone-based derivatives, i.e., 3-{5-[(Z,2Z)-2-chloro-3-(4-nitrophenyl)-2-propenylidene]-4-oxo-2-thioxothiazolidin-3-yl}propanoic acid (Les-45) and [...] Read more.
A range of hybrid molecules incorporating the ciminalum moiety in the thiazolidinone ring demonstrate significant anticancer and antimicrobial properties. Therefore, the aim of our study was to evaluate the properties and mechanism of action of two 4-thiazolidinone-based derivatives, i.e., 3-{5-[(Z,2Z)-2-chloro-3-(4-nitrophenyl)-2-propenylidene]-4-oxo-2-thioxothiazolidin-3-yl}propanoic acid (Les-45) and 5-[2-chloro-3-(4-nitrophenyl)-2-propenylidene]-2-(3-hydroxyphenylamino)thiazol-4(5H)-one (Les-247). In our study, we analyzed the impact of Les-45 and Les-247 on metabolic activity, caspase-3 activity, and the expression of genes and proteins related to inflammatory and antioxidant defenses and cytoskeleton rearrangement in healthy human fibroblasts (BJ) and a human lung carcinoma cell line (A549). The cells were exposed to increasing concentrations (1 nM to 100 μM) of the studied compounds for 24 h and 48 h. A decrease in the metabolic activity in the BJ and A549 cell lines was induced by both compounds at a concentration range from 10 to 100 µM. Both compounds decreased the mRNA expression of NRF2 (nuclear factor erythroid 2-related factor 2) and β-actin in the BJ cells. Interestingly, a significant decrease in the level of NF-κB gene and protein expression was detected in the BJ cell line, suggesting a direct impact of the studied compounds on the inhibition of inflammation. However, more studies are needed due to the ability of Les-45 and Les-247 to interfere with the tubulin/actin cytoskeleton, i.e., a critical system existing in eukaryotic cells. Full article
(This article belongs to the Special Issue Cancer: Molecular Research and Novel Inflammatory Targets)
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