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Cell Signaling and Immune Targets in Cancer
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Cell Signaling and Immune Targets in Cancer

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

Deadline for manuscript submissions: closed (31 July 2023) | Viewed by 5474

Special Issue Editors

Dr. Pierangela Totta

E-Mail Website
Guest Editor
D&V Farma Srl 00100 Rome, Rome, Italy
Interests: stem cells; cancer; cell therapy; physiology; clinical trial; cell signaling
Dr. Barbara Illi

E-Mail Website
Guest Editor
Institute of Molecular Biology and Pathology - National Research Council (IBPM-CNR), Department of Biology and Biotecnology, Sapienza University of Rome, 00185 Roma, Italy
Interests: epigenetics; stem cells (including cancer stem cells); gene expression; molecular mechanisms of tumorigenesis; transcription factors; chromatin remodelling enzymes; post-translational modifications
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cancer is a major public health problem worldwide. With over 100 different types—and great phenotypic and genotypic heterogeneity within a single cancer type—it is very difficult to provide generalized and effective therapy. Thus, research has increasingly focused on targeted therapy based on small-molecule, monoclonal antibodies, as well as developing technologies capable of modulating the immune system, such as CAR-T or CAR-NK immunotherapies.

This Special Issue aims to collect the latest findings on molecular pathways and immunology targets in cancer. Original articles reporting biomolecular studies—including pre-clinical studies—reviews, and commentaries are welcome. Pure clinical studies will not be considered for this Special Issue.

Dr. Pierangela Totta
Dr. Barbara Illi
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
  • immunotherapy
  • stem cells
  • cell signaling
  • small molecules
  • monoclonal antibodies
  • cell death
  • apostosis
  • chemoresistance
  • cell cycle
  • autophagy

Published Papers (3 papers)

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Research

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11 pages, 1979 KiB  
Article
Extra-Cellular Vesicles Derived from Thyroid Cancer Cells Promote the Epithelial to Mesenchymal Transition (EMT) and the Transfer of Malignant Phenotypes through Immune Mediated Mechanisms
by Stefania Mardente, Michele Aventaggiato, Elena Splendiani, Emanuela Mari, Alessandra Zicari, Giuseppina Catanzaro, Agnese Po, Lucia Coppola and Marco Tafani
Int. J. Mol. Sci. 2023, 24(3), 2754; https://doi.org/10.3390/ijms24032754 - 01 Feb 2023
Cited by 3 | Viewed by 1525
Abstract
Thyroid cancer is the most common endocrine cancer, and its incidence is increasing in many countries around the world. Among thyroid cancers, the papillary thyroid cancer (PTC) histotype is particularly prevalent. A small percentage of papillary tumors is associated with metastases and aggressive [...] Read more.
Thyroid cancer is the most common endocrine cancer, and its incidence is increasing in many countries around the world. Among thyroid cancers, the papillary thyroid cancer (PTC) histotype is particularly prevalent. A small percentage of papillary tumors is associated with metastases and aggressive behavior due to de-differentiation obtained through the epithelial–mesenchymal transition (EMT) by which epithelial thyroid cells acquire a fibroblast-like morphology, reduce cellular adhesion, increase motility and expression of mesenchymal proteins. The tumor microenvironment plays an important role in promoting an aggressive phenotype through hypoxia and the secretion of HMGB1 and other factors. Hypoxia has been shown to drastically change the tumor cell phenotype and has been associated with increasing metastatic and migratory behavior. Cells transfer information to neighboring cells or distant locations by releasing extracellular membrane vesicles (EVs) that contain key molecules, such as mRNAs, microRNAs (miRNAs), and proteins, that are able to modify protein expression in recipient cells. In this study, we investigated the potential role of EVs released by the anaplastic cancer cell line CAL-62 in inducing a malignant phenotype in a papillary cancer cell line (BCPAP). Full article
(This article belongs to the Special Issue Cell Signaling and Immune Targets in Cancer)
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15 pages, 3238 KiB  
Article
Analysis of Serial Neuroblastoma PDX Passages in Mice Allows the Identification of New Mediators of Neuroblastoma Aggressiveness
by María A. Gómez-Muñoz, Diana Aguilar-Morante, Ana Colmenero-Repiso, Aida Amador-Álvarez, Mónica Ojeda-Puertas, Juan Antonio Cordero Varela, Ismael Rodríguez-Prieto, Ricardo Pardal and Francisco M. Vega
Int. J. Mol. Sci. 2023, 24(2), 1590; https://doi.org/10.3390/ijms24021590 - 13 Jan 2023
Cited by 1 | Viewed by 1833
Abstract
Neuroblastoma is a neural crest cell-derived pediatric tumor characterized by high inter- and intra-tumor heterogeneity, and by a poor outcome in advanced stages. Patient-derived xenografts (PDXs) have been shown to be useful models for preserving and expanding original patient biopsies in vivo, and [...] Read more.
Neuroblastoma is a neural crest cell-derived pediatric tumor characterized by high inter- and intra-tumor heterogeneity, and by a poor outcome in advanced stages. Patient-derived xenografts (PDXs) have been shown to be useful models for preserving and expanding original patient biopsies in vivo, and for studying neuroblastoma biology in a more physiological setting. The maintenance of genetic, histologic, and phenotypic characteristics of the original biopsy along serial PDX passages in mice is a major concern regarding this model. Here we analyze consecutive PDX passages in mice, at both transcriptomic and histological levels, in order to identify potential changes or highlight similarities to the primary sample. We studied temporal changes using mRNA and miRNA expression and correlate those with neuroblastoma aggressiveness using patient-derived databases. We observed a shortening of tumor onset and an increase in proliferative potential in the PDXs along serial passages. This behavior correlates with changes in the expression of genes related to cell proliferation and neuronal differentiation, including signaling pathways described as relevant for neuroblastoma malignancy. We also identified new genes and miRNAs that can be used to stratify patients according to survival, and which could be potential new players in neuroblastoma aggressiveness. Our results highlight the usefulness of the PDX neuroblastoma model and reflect phenotypic changes that might be occurring in the mouse environment. These findings could be useful for understanding the progression of tumor aggressiveness in this pathology. Full article
(This article belongs to the Special Issue Cell Signaling and Immune Targets in Cancer)
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Review

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16 pages, 1237 KiB  
Review
CD155 and Its Receptors as Targets for Cancer Therapy
by Rossella Paolini and Rosa Molfetta
Int. J. Mol. Sci. 2023, 24(16), 12958; https://doi.org/10.3390/ijms241612958 - 19 Aug 2023
Cited by 3 | Viewed by 1653
Abstract
CD155, also known as the poliovirus receptor, is an adhesion molecule often overexpressed in tumors of different origins where it promotes cell migration and proliferation. In addition to this pro-tumorigenic function, CD155 plays an immunomodulatory role during tumor progression since it is a [...] Read more.
CD155, also known as the poliovirus receptor, is an adhesion molecule often overexpressed in tumors of different origins where it promotes cell migration and proliferation. In addition to this pro-tumorigenic function, CD155 plays an immunomodulatory role during tumor progression since it is a ligand for both the activating receptor DNAM-1 and the inhibitory receptor TIGIT, expressed on cytotoxic innate and adaptative lymphocytes. DNAM-1 is a well-recognized receptor involved in anti-tumor immune surveillance. However, in advanced tumor stages, TIGIT is up-regulated and acts as an immune checkpoint receptor, counterbalancing DNAM-1-mediated cancer cell clearance. Pre-clinical studies have proposed the direct targeting of CD155 on tumor cells as well as the enhancement of DNAM-1-mediated anti-tumor functions as promising therapeutic approaches. Moreover, immunotherapeutic use of anti-TIGIT blocking antibody alone or in combined therapy has already been included in clinical trials. The aim of this review is to summarize all these potential therapies, highlighting the still controversial role of CD155 during tumor progression. Full article
(This article belongs to the Special Issue Cell Signaling and Immune Targets in Cancer)
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