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Ephrin Receptors and Cancer 2.0
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Ephrin Receptors and Cancer 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 (31 December 2022) | Viewed by 5932

Special Issue Editor

Prof. Dr. Stamatios E. Theocharis

E-Mail Website
Guest Editor
First Department of Pathology, School of Medicine, National and Kapodistrian University of Athens, 11527 Athens, Greece
Interests: cancer pathology; cancer biomarker; cancer diagnosis; cancer prognosis; nutritional intervention in cancer clinical and experimental studies
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The family of receptor tyrosine kinases (RTKs), ephrin receptors (EPHs), comprises 14 cell-bound members divided into two classes, A and B, based on their sequence similarity and binding affinity to their ligands, ephrins. In a similar manner, ephrins are also cell-bound proteins and include ephrin-A and ephrin-B classes. Nine class A EPHs (EPHA1-EPHA8, EPHA10) and five class B EPHs (EPHB1-EPHB4, EPHB6) preferentially bind five ephrin-A and three ephrin-B classes. The EPH/ephrin system is involved into key regulatory processes of human physiology: it highlights axon guidance and synaptic plasticity in the nervous system, as well as angiogenesis, vascular remodeling, and homeostasis of various tissues. In addition, this cell–cell communication system is implicated in several pathologic processes, including neurodegenerative disorders, viral infections, and cancer. Indeed, its deregulation affects tumor growth, progression, metastasis, and neovascularization by disrupting critical signaling transduction pathways. EPHs’ and ephrins’ aberrant expression characterizes not only the tumor cells but also the tumor microenvironment, where endothelial cells have mostly been investigated; this makes the EPH/ephrin system an appealing candidate for targeted intervention. EPHs’ upregulation in the pathogenesis of malignant transformation has been reported, suggesting their use as potential biomarkers and drug targets for various cancer types.

Prof. Dr. Stamatios E. Theocharis
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

  • ephrin receptors
  • ephrins
  • cancer
  • pathogenesis
  • biomarkers
  • treatment

Published Papers (3 papers)

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Research

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22 pages, 4887 KiB  
Article
Novel Isoform DTX3c Associates with UBE2N-UBA1 and Cdc48/p97 as Part of the EphB4 Degradation Complex Regulated by the Autocrine IGF-II/IRA Signal in Malignant Mesothelioma
by Pierluigi Scalia, Carmen Merali, Carlos Barrero, Antonio Suma, Vincenzo Carnevale, Salim Merali and Stephen J. Williams
Int. J. Mol. Sci. 2023, 24(8), 7380; https://doi.org/10.3390/ijms24087380 - 17 Apr 2023
Cited by 3 | Viewed by 1576
Abstract
EphB4 angiogenic kinase over-expression in Mesothelioma cells relies upon a degradation rescue signal provided by autocrine IGF-II activation of Insulin Receptor A. However, the identity of the molecular machinery involved in EphB4 rapid degradation upon IGF-II signal deprivation are unknown. Using targeted proteomics, [...] Read more.
EphB4 angiogenic kinase over-expression in Mesothelioma cells relies upon a degradation rescue signal provided by autocrine IGF-II activation of Insulin Receptor A. However, the identity of the molecular machinery involved in EphB4 rapid degradation upon IGF-II signal deprivation are unknown. Using targeted proteomics, protein–protein interaction methods, PCR cloning, and 3D modeling approaches, we identified a novel ubiquitin E3 ligase complex recruited by the EphB4 C tail upon autocrine IGF-II signal deprivation. We show this complex to contain a previously unknown N-Terminal isoform of Deltex3 E3-Ub ligase (referred as “DTX3c”), along with UBA1(E1) and UBE2N(E2) ubiquitin ligases and the ATPase/unfoldase Cdc48/p97. Upon autocrine IGF-II neutralization in cultured MSTO211H (a Malignant Mesothelioma cell line that is highly responsive to the EphB4 degradation rescue IGF-II signal), the inter-molecular interactions between these factors were enhanced and their association with the EphB4 C-tail increased consistently with the previously described EphB4 degradation pattern. The ATPase/unfoldase activity of Cdc48/p97 was required for EphB4 recruitment. As compared to the previously known isoforms DTX3a and DTX3b, a 3D modeling analysis of the DTX3c Nt domain showed a unique 3D folding supporting isoform-specific biological function(s). We shed light on the molecular machinery associated with autocrine IGF-II regulation of oncogenic EphB4 kinase expression in a previously characterized IGF-II+/EphB4+ Mesothelioma cell line. The study provides early evidence for DTX3 Ub-E3 ligase involvement beyond the Notch signaling pathway. Full article
(This article belongs to the Special Issue Ephrin Receptors and Cancer 2.0)
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Review

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13 pages, 1005 KiB  
Review
The EPH/Ephrin System in Pancreatic Ductal Adenocarcinoma (PDAC): From Pathogenesis to Treatment
by Stavros P. Papadakos, Nikolaos Dedes, Nikolina Gkolemi, Nikolaos Machairas and Stamatios Theocharis
Int. J. Mol. Sci. 2023, 24(3), 3015; https://doi.org/10.3390/ijms24033015 - 03 Feb 2023
Cited by 6 | Viewed by 1970
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is a major concern for health care systems worldwide, since its mortality remains unaltered despite the surge in cutting-edge science. The EPH/ephrin signaling system was first investigated in the 1980s. EPH/ephrins have been shown to exert bidirectional signaling and [...] Read more.
Pancreatic ductal adenocarcinoma (PDAC) is a major concern for health care systems worldwide, since its mortality remains unaltered despite the surge in cutting-edge science. The EPH/ephrin signaling system was first investigated in the 1980s. EPH/ephrins have been shown to exert bidirectional signaling and cell-to-cell communication, influencing cellular morphology, adhesion, migration and invasion. Recent studies have highlighted the critical role of the EPH/ephrin system in various physiologic processes, including cellular proliferation, survival, synaptic plasticity and angiogenesis. Thus, it has become evident that the EPH/ephrin signaling system may have compelling effects on cell homeostasis that contribute to carcinogenesis. In particular, the EPH/ephrins have an impact on pancreatic morphogenesis and development, whereas several EPHs and ephrins are altered in PDAC. Several clinical and preclinical studies have attempted to elucidate the effects of the EPH/ephrin pathway, with multilayered effects on PDAC development. These studies have highlighted its highly promising role in the diagnosis, prognosis and therapeutic management of PDAC. The aim of this review is to explore the obscure aspects of the EPH/ephrin system concerning the development, physiology and homeostasis of the pancreas. Full article
(This article belongs to the Special Issue Ephrin Receptors and Cancer 2.0)
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9 pages, 651 KiB  
Review
EPH/Ephrin-Targeting Treatment in Breast Cancer: A New Chapter in Breast Cancer Therapy
by Iason Psilopatis, Eleni Souferi-Chronopoulou, Kleio Vrettou, Constantinos Troungos and Stamatios Theocharis
Int. J. Mol. Sci. 2022, 23(23), 15275; https://doi.org/10.3390/ijms232315275 - 03 Dec 2022
Cited by 7 | Viewed by 1891
Abstract
Breast cancer (BC) is the most common malignant tumor in women. Erythropoietin-producing hepatocellular receptors (EPHs), receptor tyrosine kinases binding the membrane-bound proteins ephrins, are differentially expressed in BC, and correlate with carcinogenesis and tumor progression. With a view to examining available therapeutics targeting [...] Read more.
Breast cancer (BC) is the most common malignant tumor in women. Erythropoietin-producing hepatocellular receptors (EPHs), receptor tyrosine kinases binding the membrane-bound proteins ephrins, are differentially expressed in BC, and correlate with carcinogenesis and tumor progression. With a view to examining available therapeutics targeting the EPH/ephrin system in BC, a literature review was conducted, using the MEDLINE, LIVIVO, and Google Scholar databases. EPHA2 is the most studied EPH/ephrin target in BC treatment. The targeting of EPHA2, EPHA10, EPHB4, ephrin-A2, ephrin-A4, as well as ephrin-B2 in BC cells or xenograft models is associated with apoptosis induction, tumor regression, anticancer immune response activation, and impaired cell motility. In conclusion, EPHs/ephrins seem to represent promising future treatment targets in BC. Full article
(This article belongs to the Special Issue Ephrin Receptors and Cancer 2.0)
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