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  1. Cancers
  2. Volume: 8
  3. Issue: 6
  4. Control of Wnt Receptor Turnover by R-spondin-ZNRF3/RNF43 Signaling Module and Its Dysregulation in Cancer
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Volume: 10
Volume: 9
Volume: 8
Issue: 12
Issue: 11
Issue: 10
Issue: 9
Issue: 8
Issue: 7
Issue: 6
Tomato as a Source of Carotenoids and Polyphenols Targeted to Cancer Prevention
S100A4 in Cancer Metastasis: Wnt Signaling-Driven Interventions for Metastasis Restriction
Wnt Signaling in Renal Cell Carcinoma
Targeted Vaccination against Human α-Lactalbumin for Immunotherapy and Primary Immunoprevention of Triple Negative Breast Cancer
RASSF1A Site-Specific Methylation Hotspots in Cancer and Correlation with RASSF1C and MOAP-1
Control of Wnt Receptor Turnover by R-spondin-ZNRF3/RNF43 Signaling Module and Its Dysregulation in Cancer
Letter to the Editor Re: Ogawa, Y. Cancers 2016, 8, 28
Issue: 5
Issue: 4
Issue: 3
Issue: 2
Issue: 1
Volume: 7
Volume: 6
Volume: 5
Volume: 4
Volume: 3
Volume: 2
Volume: 1

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Control of Wnt Receptor Turnover by R-spondin-ZNRF3/RNF43 Signaling Module and Its Dysregulation in Cancer

Content Provider MDPI
Author Hao, Huai-Xiang Jiang, Xiaomo Cong, Feng
Abstract Aberrant activation of the Wnt/β-catenin pathway is frequently found in various cancers, often through mutations of downstream components. Inhibiting β-catenin signaling in tumors with downstream pathway mutations remains challenging, due to a lack of favorable targets. On the other hand, targeting upstream components of the Wnt pathway is rather straightforward. However, it is difficult to identify tumors addicted to autocrine or paracrine Wnt signaling. Discovery of the R-spondin-ZNRF3/RNF43 signaling module and its genetic alterations in cancers represents a breakthrough in this area. Membrane E3 ligase ZNRF3 and RNF43 are critical negative feedback regulators of the Wnt pathway, which function through promoting ubiquitination and degradation of Wnt receptors. R-spondin proteins (RSPO1-4) serve as natural antagonists of ZNRF3/RNF43. To maintain strong and sustained Wnt/β-catenin signaling, cancers need to overcome ZNRF3/RNF43-mediated feedback inhibition. Indeed, mutations of RNF43/ZNRF3 and recurrent translocations of RSPO2/RSPO3 have recently been identified in various cancers. Significantly, genetic alterations in RNF43/ZNRF3/RSPO2/RSPO3 have shown promise as predictive biomarkers in pre-clinical models for the efficacy of upstream Wnt inhibitors. In this review, we will discuss the biology of the R-spondin-ZNRF3/RNF43 signaling module, cancer-associated alterations of this signaling module, and their value as biomarkers to identify Wnt-addicted tumors.
File Size 551936
File Format PDF
e-ISSN 20726694
DOI 10.3390/cancers8060054
Journal Cancers
Issue Number 6
Volume Number 8
Language English
Publisher Date 2016-06-08
Access Restriction Open
Subject Keyword Wnt signaling pathway targeted therapy RNF43 ZNRF3 R-spondin Frizzled
Content Type Text
Resource Type Article
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