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WWC3 Inhibits Glioma Cell Proliferation Through Suppressing the Wnt/β-Catenin Signaling Pathway.

Authors
  • Wang, Yanni1
  • Jiang, Man2
  • Yao, Yongshan3
  • Cai, Zhengwei1
  • 1 1 Department of Pediatrics, The First College of Clinical Medical Science, China Three Gorges University , Yi Chang City, China . , (China)
  • 2 2 Department of Emergency, The First College of Clinical Medical Science, China Three Gorges University , Yi Chang City, China . , (China)
  • 3 3 Department of Emergency and Traumatic Surgery, The First College of Clinical Medical Science, China Three Gorges University , Yi Chang City, China . , (China)
Type
Published Article
Journal
DNA and Cell Biology
Publisher
Mary Ann Liebert
Publication Date
Nov 08, 2017
Identifiers
DOI: 10.1089/dna.2017.3931
PMID: 29115863
Source
Medline
Keywords
License
Unknown

Abstract

The scaffolding protein WW and C2 domain-containing protein 3 (WWC3) belonging to the WWC protein family plays important roles in regulating cell proliferation, cell migration, and synaptic signaling. The critical role of WWC3 in tumorigenesis has emerged recently; however, the expression and function of WWC3 in glioma remain largely unknown. Here, we found that WWC3 was significantly downregulated in glioma tissues and cell lines. Overexpression of WWC3 inhibited the glioma cell proliferation, migration, and invasion. Depletion of WWC3 promoted the proliferation of glioma cells. Mechanistically, we found that overexpression of WWC3 suppressed the activity of β-catenin, the signaling that tightly associates with cell proliferation and growth. Depletion of WWC3 enhanced the activity of β-catenin/Wnt signaling. Further investigation demonstrated that WWC3 interacted with T cell factor 4 (TCF4), an identified associated binding partner of β-catenin. The interaction between WWC3 and TCF4 might inhibit the transcriptional activation of β-catenin. Our results provide novel insights into the aberrant expression and molecular mechanism of WWC3 in glioma, which indicated WWC3 as a potential target for clinical intervention in glioma.

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