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Special Issue "The Wnt Signaling Pathway in Cancer"

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 May 2020).

Special Issue Editor

Assoc. Prof. Dr. Yong-mi Kim
Website
Guest Editor
Keck School of Medicine, University of Southern California; USAUniversity of Southern California, Department of Pediatrics, Los Angeles, USA
Interests: acute lymphoblastic leukemia; drug resistance; microenvironment; integrins; wnt signaling; immunotherapy resistance

Special Issue Information

Dear Colleagues,

This Special Issue focuses on the Wnt Signaling Pathway in Cancer. Wnt signaling has been of considerable interest in both setm cell and cancer biology, both in homeostatic maintenance of tissues and organs through their respective somatic stem cells (SSCs) and in cancer stem cells (CSCs). The functions include cellular processes, including self-renewal capacity, proliferation, differentiation potential, and maintenance of the stem cell niche. The role of aberrant wnt signaling in cancer stem cells (CSCs) has been demonstrated in a wide variety of cancers, including brain tumors, melanoma, breast, liver, pancreatic, and colon cancer, but also hematological malignancies. Wnt siangling has been shown to be involved in initiation of disease, therapeutic resistance, and ultimately, disease relapse. One key focus in cancer research has been to develop therapies to safely eliminate CSCs. The precise understanding of the regulation of wnt signaling, the crosstalk of wnt signaling with other signaling pathways, and downstream targets are key for successful translational efforts, which will be the focus of this Special Edition. Original investigations as well as concise review manuscripts from experts in the relevant research fields will be considered for publication.

Assoc. Prof. Dr. Yong-mi Kim
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 papers will be 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

  • Wnt
  • Cancer
  • Drug resistance
  • Therapy
  • Microenvironment
  • Self-renewal
  • Differentiation

Published Papers (4 papers)

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Research

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Open AccessArticle
LY75 Ablation Mediates Mesenchymal-Epithelial Transition (MET) in Epithelial Ovarian Cancer (EOC) Cells Associated with DNA Methylation Alterations and Suppression of the Wnt/β-Catenin Pathway
Int. J. Mol. Sci. 2020, 21(5), 1848; https://doi.org/10.3390/ijms21051848 - 07 Mar 2020
Abstract
Growing evidence demonstrates that epithelial–mesenchymal transition (EMT) plays an important role in epithelial ovarian cancer (EOC) progression and spreading; however, its molecular mechanisms remain poorly defined. We have previously shown that the antigen receptor LY75 can modulate EOC cell phenotype and metastatic potential, [...] Read more.
Growing evidence demonstrates that epithelial–mesenchymal transition (EMT) plays an important role in epithelial ovarian cancer (EOC) progression and spreading; however, its molecular mechanisms remain poorly defined. We have previously shown that the antigen receptor LY75 can modulate EOC cell phenotype and metastatic potential, as LY75 depletion directed mesenchymal–epithelial transition (MET) in EOC cell lines with mesenchymal phenotype. We used the LY75-mediated modulation of EMT as a model to investigate for DNA methylation changes during EMT in EOC cells, by applying the reduced representation bisulfite sequencing (RRBS) methodology. Numerous genes have displayed EMT-related DNA methylation patterns alterations in their promoter/exon regions. Ten selected genes, whose DNA methylation alterations were further confirmed by alternative methods, were further identified, some of which could represent new EOC biomarkers/therapeutic targets. Moreover, our methylation data were strongly indicative for the predominant implication of the Wnt/β-catenin pathway in the EMT-induced DNA methylation variations in EOC cells. Consecutive experiments, including alterations in the Wnt/β-catenin pathway activity in EOC cells with a specific inhibitor and the identification of LY75-interacting partners by a proteomic approach, were strongly indicative for the direct implication of the LY75 receptor in modulating the Wnt/β-catenin signaling in EOC cells. Full article
(This article belongs to the Special Issue The Wnt Signaling Pathway in Cancer)
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Review

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Open AccessReview
Wnt/β-Catenin Signaling in Oral Carcinogenesis
Int. J. Mol. Sci. 2020, 21(13), 4682; https://doi.org/10.3390/ijms21134682 - 30 Jun 2020
Abstract
Oral carcinogenesis is a complex and multifactorial process that involves cumulative genetic and molecular alterations, leading to uncontrolled cell proliferation, impaired DNA repair and defective cell death. At the early stages, the onset of potentially malignant lesions in the oral mucosa, or oral [...] Read more.
Oral carcinogenesis is a complex and multifactorial process that involves cumulative genetic and molecular alterations, leading to uncontrolled cell proliferation, impaired DNA repair and defective cell death. At the early stages, the onset of potentially malignant lesions in the oral mucosa, or oral dysplasia, is associated with higher rates of malignant progression towards carcinoma in situ and invasive carcinoma. Efforts have been made to get insights about signaling pathways that are deregulated in oral dysplasia, as these could be translated into novel markers and might represent promising therapeutic targets. In this context, recent evidence underscored the relevance of the Wnt/β-catenin signaling pathway in oral dysplasia, as this pathway is progressively “switched on” through the different grades of dysplasia (mild, moderate and severe dysplasia), with the consequent nuclear translocation of β-catenin and expression of target genes associated with the maintenance of representative traits of oral dysplasia, namely cell proliferation and viability. Intriguingly, recent studies provide an unanticipated connection between active β-catenin signaling and deregulated endosome trafficking in oral dysplasia, highlighting the relevance of endocytic components in oral carcinogenesis. This review summarizes evidence about the role of the Wnt/β-catenin signaling pathway and the underlying mechanisms that account for its aberrant activation in oral carcinogenesis. Full article
(This article belongs to the Special Issue The Wnt Signaling Pathway in Cancer)
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Open AccessReview
Wnt Signaling in Gynecologic Malignancies
Int. J. Mol. Sci. 2020, 21(12), 4272; https://doi.org/10.3390/ijms21124272 - 16 Jun 2020
Abstract
Gynecologic malignancies, including ovarian cancer, endometrial cancer, and cervical cancer, affect hundreds of thousands of women worldwide every year. Wnt signaling, specifically Wnt/β-catenin signaling, has been found to play an essential role in many oncogenic processes in gynecologic malignancies, including tumorigenesis, metastasis, recurrence, [...] Read more.
Gynecologic malignancies, including ovarian cancer, endometrial cancer, and cervical cancer, affect hundreds of thousands of women worldwide every year. Wnt signaling, specifically Wnt/β-catenin signaling, has been found to play an essential role in many oncogenic processes in gynecologic malignancies, including tumorigenesis, metastasis, recurrence, and chemotherapy resistance. As such, the Wnt/β-catenin signaling pathway has the potential to be a target for effective treatment, improving patient outcomes. In this review, we discuss the evidence supporting the importance of the Wnt signaling pathways in the development, progression, and treatment of gynecologic malignancies. Full article
(This article belongs to the Special Issue The Wnt Signaling Pathway in Cancer)
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Open AccessReview
Targeting Wnt Signaling for the Treatment of Gastric Cancer
Int. J. Mol. Sci. 2020, 21(11), 3927; https://doi.org/10.3390/ijms21113927 - 30 May 2020
Abstract
The Wnt signaling pathway is evolutionarily conserved, regulating both embryonic development and maintaining adult tissue homeostasis. Wnt signaling controls several fundamental cell functions, including proliferation, differentiation, migration, and stemness. It therefore plays an important role in the epithelial homeostasis and regeneration of the [...] Read more.
The Wnt signaling pathway is evolutionarily conserved, regulating both embryonic development and maintaining adult tissue homeostasis. Wnt signaling controls several fundamental cell functions, including proliferation, differentiation, migration, and stemness. It therefore plays an important role in the epithelial homeostasis and regeneration of the gastrointestinal tract. Often, both hypo- or hyper-activation of the pathway due to genetic, epigenetic, or receptor/ligand alterations are seen in many solid cancers, such as breast, colorectal, gastric, and prostate. Gastric cancer (GC) is the fourth commonest cause of cancer worldwide and is the second leading cause of cancer-related death annually. Although the number of new diagnoses has declined over recent decades, prognosis remains poor, with only 15% surviving to five years. Geographical differences in clinicopathological features are also apparent, with epidemiological and genetic studies revealing GC to be a highly heterogeneous disease with phenotypic diversity as a result of etiological factors. The molecular heterogeneity associated with GC dictates that a single ‘one size fits all’ approach to management is unlikely to be successful. Wnt pathway dysregulation has been observed in approximately 50% of GC tumors and may offer a novel therapeutic target for patients who would otherwise have a poor outcome. This mini review will highlight some recent discoveries involving Wnt signaling in GC. Full article
(This article belongs to the Special Issue The Wnt Signaling Pathway in Cancer)
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