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From Mechanisms to Therapeutics: Wnt Signaling in Cancer—Second Edition
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From Mechanisms to Therapeutics: Wnt Signaling in Cancer—Second Edition

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 15 September 2024 | Viewed by 969

Special Issue Editors

Dr. Anitha K. Shenoy

E-Mail Website
Guest Editor
Department of Pharmaceutical and Biomedical Sciences, College of Pharmacy, California Health Sciences University, Clovis, California, USA
Interests: Wnt signaling; signal transduction; cancer biology; stem cells; cancer stem cells; angiogenesis
Special Issues, Collections and Topics in MDPI journals
Dr. Liya Pi

E-Mail Website
Guest Editor
Department of Pathology and Laboratory Medicine, Tulane University, New Orleans, LA 70112, USA
Interests: hepatic progenitor cell activation; liver regeneration; alcoholic fibrosis; liver cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The Wnt signaling pathway plays a central role in human development, tissue homeostasis, and a plethora of diseases including cancer.  It is well-recognized that the canonical as well as non-canonical Wnt signaling pathways are closely associated with tumor initiation, progression, and metastasis. The canonical Wnt signaling also regulates the formation and maintenance of embryonic, adult, and cancer stem cells. In addition, there exists a complex relationship between Wnt signaling and the tumor microenvironment that promotes cancer cell proliferation.  As a result, the Wnt signaling pathway and its components have become attractive drug targets for cancer treatment.

However, cancer drug development efforts aimed at Wnt signaling have been largely unsuccessful due to the ubiquitous nature of this pathway in health and disease. A thorough understanding of the Wnt mechanism in cancer pathophysiology, its role in conferring drug resistance, and the impact of its inhibition on cancer treatment are warranted to develop effective therapeutic strategies. In this regard, we welcome original articles and reviews for this Special Issue. Topics of interest include, but are not limited to, the following:

  1. Wnt signaling in tumorigenesis and development of cancer;
  2. Targeting Wnt signaling in cancer;
  3. Wnt signaling and drug resistance in cancer;
  4. Wnt signaling and the tumor microenvironment;
  5. Wnt signaling and cancer stem cells;
  6. Strategies to employ Wnt signaling pathway modulators in cancer treatment.

Dr. Anitha K. Shenoy
Dr. Liya Pi
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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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
  • β-catenin
  • development
  • homeostasis
  • cancer
  • cancer stem cells (CSC)
  • targeted cancer therapy
  • canonical Wnt signaling
  • non-canonical Wnt signaling

Related Special Issue

Published Papers (1 paper)

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Research

17 pages, 1910 KiB  
Article
Synthetic Lethality between Cohesin and WNT Signaling Pathways in Diverse Cancer Contexts
by Maria Michela Pallotta, Maddalena Di Nardo and Antonio Musio
Cells 2024, 13(7), 608; https://doi.org/10.3390/cells13070608 - 30 Mar 2024
Viewed by 754
Abstract
Cohesin is a highly conserved ring-shaped complex involved in topologically embracing chromatids, gene expression regulation, genome compartmentalization, and genome stability maintenance. Genomic analyses have detected mutations in the cohesin complex in a wide array of human tumors. These findings have led to increased [...] Read more.
Cohesin is a highly conserved ring-shaped complex involved in topologically embracing chromatids, gene expression regulation, genome compartmentalization, and genome stability maintenance. Genomic analyses have detected mutations in the cohesin complex in a wide array of human tumors. These findings have led to increased interest in cohesin as a potential target in cancer therapy. Synthetic lethality has been suggested as an approach to exploit genetic differences in cancer cells to influence their selective killing. In this study, we show that mutations in ESCO1, NIPBL, PDS5B, RAD21, SMC1A, SMC3, STAG2, and WAPL genes are synthetically lethal with stimulation of WNT signaling obtained following LY2090314 treatment, a GSK3 inhibitor, in several cancer cell lines. Moreover, treatment led to the stabilization of β-catenin and affected the expression of c-MYC, probably due to the occupancy decrease in cohesin at the c-MYC promoter. Finally, LY2090314 caused gene expression dysregulation mainly involving pathways related to transcription regulation, cell proliferation, and chromatin remodeling. For the first time, our work provides the underlying molecular basis for synthetic lethality due to cohesin mutations and suggests that targeting the WNT may be a promising therapeutic approach for tumors carrying mutated cohesin. Full article
(This article belongs to the Special Issue From Mechanisms to Therapeutics: Wnt Signaling in Cancer—Second Edition)
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