Wnt Pathway Targets in Cancer

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Pathophysiology".

Deadline for manuscript submissions: closed (20 December 2023) | Viewed by 9552

Special Issue Editors

Department of Molecular Medicine, Beckman Research Institute of City of Hope, Duarte, CA 91010, USA
Interests: Wnt signaling; cancers of liver and pancreas; metabolism; fibrosis
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Guest Editor
Department of Applied Biology and Chemical Technology, The Hong Kong Polytechnic University, Hong Kong 999077, China
Interests: drug resistance; hepatocellular carcinoma; gut microbiota; immune resistance; tumor microenvironment
Department of Medicine, University of California, San Francisco (UCSF), San Francisco, CA 94143, USA
Interests: Wnt signaling; liver cancer; liver development; adult hepatocyte stem cells; liver cell atlas; acute hepatic porphyrias

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Guest Editor
Department of Pathology and Laboratory Medicine, University of California, Los Angeles (UCLA), Los Angeles, CA 90095, USA
Interests: Wnt signaling; Kras signaling; pancreatic cancer; chemoprevention, early detection and therapeutic approaches

Special Issue Information

Dear Colleagues,

Dysregulation of Wnt signaling is known to be associated with various cancers. As such, identification of novel Wnt pathway targets in cancer and better characterization of already-known targets present exciting, emerging opportunities for cancer treatment and perhaps even prevention. In this Special Issue, we propose to cover Wnt pathway targets in cancer, with a focus on solid tumors, especially highly lethal cancers of the liver (e.g., HCC), pancreas (e.g., PDAC), and GI tract. Topics may include but are not limited to the role(s) of Wnt pathway targets in cancer stem cells, nonparenchymal cells, cancer metabolism, tumor immune response, and tumor microenvironment. Original research articles, review articles, as well as short communications are invited for this Special Issue.

We look forward to receiving your contributions.

Dr. Keane Lai
Dr. Terence K.W. Lee
Dr. Bruce Wang
Dr. David W. Dawson
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. Cancers 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 2900 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
  • cancer
  • liver
  • pancreas
  • gastrointestinal tract
  • hepatocellular carcinoma
  • pancreatic ductal adenocarcinoma
  • gastric cancer
  • colon cancer
  • solid tumors

Published Papers (4 papers)

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Research

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12 pages, 2755 KiB  
Article
Responses to the Tepotinib in Gastric Cancers with MET Amplification or MET Exon 14 Skipping Mutations and High Expression of Both PD-L1 and CD44
by Sung-Hwa Sohn, Hee Jung Sul, Bum Jun Kim and Dae Young Zang
Cancers 2022, 14(14), 3444; https://doi.org/10.3390/cancers14143444 - 15 Jul 2022
Cited by 5 | Viewed by 1920
Abstract
Both MET exon 14 skipping mutation (METex14SM) and high copy-number variation (CNV) lead to enhanced carcinogenesis; additionally, programmed-death ligand 1 (PD-L1) is often upregulated in cancers. In this study, we characterized the expression of MET (including METex14SM), PD-L1, and CD44 in human gastric [...] Read more.
Both MET exon 14 skipping mutation (METex14SM) and high copy-number variation (CNV) lead to enhanced carcinogenesis; additionally, programmed-death ligand 1 (PD-L1) is often upregulated in cancers. In this study, we characterized the expression of MET (including METex14SM), PD-L1, and CD44 in human gastric cancer (GC) cells as well as the differential susceptibility of these cells to tepotinib. Tepotinib treatments inhibited the growth of five GC cells in a dose-dependent manner with a concomitant induction of cell death. Tepotinib treatments also significantly reduced the expression of phospho-MET, total MET, c-Myc, VEGFR2, and Snail protein in SNU620, MKN45, and Hs746T cells. Notably, tepotinib significantly reduced the expression of CD44 and PD-L1 in METex14SM Hs746T cells. By contrast, tepotinib was only slightly active against SNU638 and KATO III cells. Migration was reduced to a greater extent in the tepotinib-treated group than in the control group. Tepotinib may have therapeutic effects on c-MET-amplified GC, a high expression of both PD-L1 and CD44, and METex14SM. Clinical studies are needed to confirm these therapeutic effects. Full article
(This article belongs to the Special Issue Wnt Pathway Targets in Cancer)
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Review

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15 pages, 1314 KiB  
Review
Extracellular Vesicles Act as Carriers for Cargo Delivery and Regulate Wnt Signaling in the Hepatocellular Carcinoma Tumor Microenvironment
by Risheng He, Yi Xu, Liang Yu, Nanfeng Meng, Hang Wang, Yunfu Cui and Judy Wai Ping Yam
Cancers 2023, 15(7), 2088; https://doi.org/10.3390/cancers15072088 - 31 Mar 2023
Cited by 1 | Viewed by 1742
Abstract
As the primary type of liver cancer, hepatocellular carcinoma (HCC) causes a large number of deaths every year. Despite extensive research conducted on this disease, the prognosis of HCC remains unclear. Recently, research has largely focused on extracellular vesicles (EVs), and they have [...] Read more.
As the primary type of liver cancer, hepatocellular carcinoma (HCC) causes a large number of deaths every year. Despite extensive research conducted on this disease, the prognosis of HCC remains unclear. Recently, research has largely focused on extracellular vesicles (EVs), and they have been found to participate in various ways in the development of various diseases, including HCC, such as by regulating cell signaling pathways. However, recent studies have reported the mechanisms underlying the regulation of Wnt signaling by EVs in HCC, primarily focusing on the regulation of the canonical pathways. This review summarizes the current literature on the regulation of Wnt signaling by EVs in HCC and their underlying mechanisms. In addition, we also present future research directions in this field. This will deepen the understanding of HCC and provide new ideas for its treatment. Full article
(This article belongs to the Special Issue Wnt Pathway Targets in Cancer)
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15 pages, 2353 KiB  
Review
Low-Grade Ovarian Stromal Tumors with Genetic Alterations of the Wnt/β-Catenin Pathway That Is Crucial in Ovarian Follicle Development and Regulation
by Gloria Zhang, Chad M. Michener and Bin Yang
Cancers 2022, 14(22), 5622; https://doi.org/10.3390/cancers14225622 - 16 Nov 2022
Cited by 3 | Viewed by 1585
Abstract
The Wnt signaling pathway is important in the normal development and regulation of ovarian follicles throughout the lifecycle of females. Dysregulation of the Wnt signaling pathway, genetically or epigenetically, with subsequent activation of β-catenin has been implicated in tumorigenesis of a spectrum of [...] Read more.
The Wnt signaling pathway is important in the normal development and regulation of ovarian follicles throughout the lifecycle of females. Dysregulation of the Wnt signaling pathway, genetically or epigenetically, with subsequent activation of β-catenin has been implicated in tumorigenesis of a spectrum of ovarian neoplasms, from benign to malignant. We review the recent findings of the Wnt signaling pathway involved in regulating normal physiologic processes of the ovarian follicle cycle. We also review the β-catenin mutations in a family of low-grade ovarian stromal tumors, focusing on characterizing their shared morphological features and the utility of immunohistochemistry of β-catenin in facilitating the accurate diagnosis of these ovarian stromal tumors. The Wnt signaling pathway is one of the most critical mechanisms in regulating cell proliferation, differentiation, and morphogenesis. The Wnt signaling pathway comprises a diverse group of glycoproteins that serve as ligands and bind to transmembrane Frizzled family receptors. The ligand-receptor interactions activate the pathway and govern the downstream signaling cascades, ultimately affecting the transcriptional control of the cellular cytoskeleton, organelle dynamics, epithelial-mesenchymal interaction, and tissue remodeling in the ovary. Wnt signaling consists of two major pathways: a canonical pathway that is β-catenin-dependent and a non-canonical Wnt pathway that is β-catenin-independent. Canonical Wnt signaling is governed by the interaction of β-catenin with other molecules to regulate cellular decisions related to proliferation and differentiation. Recent studies have demonstrated that the Wnt signaling pathway plays important roles in the development and regulation of ovarian folliculogenesis and oogenesis. Full article
(This article belongs to the Special Issue Wnt Pathway Targets in Cancer)
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26 pages, 2070 KiB  
Review
Wnt/β-Catenin Signaling as a Driver of Stemness and Metabolic Reprogramming in Hepatocellular Carcinoma
by Rainbow Wing Hei Leung and Terence Kin Wah Lee
Cancers 2022, 14(21), 5468; https://doi.org/10.3390/cancers14215468 - 07 Nov 2022
Cited by 11 | Viewed by 3610
Abstract
Hepatocellular carcinoma (HCC) is a major cause of cancer death worldwide due to its high rates of tumor recurrence and metastasis. Aberrant Wnt/β-catenin signaling has been shown to play a significant role in HCC development, progression and clinical impact on tumor behavior. Accumulating [...] Read more.
Hepatocellular carcinoma (HCC) is a major cause of cancer death worldwide due to its high rates of tumor recurrence and metastasis. Aberrant Wnt/β-catenin signaling has been shown to play a significant role in HCC development, progression and clinical impact on tumor behavior. Accumulating evidence has revealed the critical involvement of Wnt/β-catenin signaling in driving cancer stemness and metabolic reprogramming, which are regarded as emerging cancer hallmarks. In this review, we summarize the regulatory mechanism of Wnt/β-catenin signaling and its role in HCC. Furthermore, we provide an update on the regulatory roles of Wnt/β-catenin signaling in metabolic reprogramming, cancer stemness and drug resistance in HCC. We also provide an update on preclinical and clinical studies targeting Wnt/β-catenin signaling alone or in combination with current therapies for effective cancer therapy. This review provides insights into the current opportunities and challenges of targeting this signaling pathway in HCC. Full article
(This article belongs to the Special Issue Wnt Pathway Targets in Cancer)
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