ArticleDigestive diseases and sciences2019
WDR34 Activates Wnt/Beta-Catenin Signaling in Hepatocellular Carcinoma.
Article in Digestive diseases and sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- The role of the WD40-repeat protein family in cancer.Molecular cancer · 2026Review
- The roles of cytoplasmic dynein complex in various ocular disorders.Molecular medicine (Cambridge, Mass.) · 2026Review
- Rod-Cone Dystrophy Related WDR34 Is Essential for Ciliary Integrity and Survival of Mammalian Photoreceptor Cells.Investigative ophthalmology & visual science · 2026Article
- High Throughput Transcriptome Data Analysis and Computational Verification Reveal Immunotherapy Biomarkers of Compound Kushen Injection for Treating Triple-Negative Breast Cancer.Frontiers in oncology · 2021Article
- WDR34 mutation from anencephaly patients impaired both SHH and PCP signaling pathways.Journal of human genetics · 2020Article
- Long non-coding RNA ROR1-AS1 induces tumorigenesis of colorectal cancer by affecting Wnt/β-catenin signaling pathway.Bioscience reports · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWnt ligand binding initiates the interaction between Frizzled and Dvl proteins. However, the regulation of Frizzled-Dvl proteins interaction remains largely unknown.
aimsThe present study aims to elucidate the regulation of Frizzled-Dvl interaction by WDR34.
methodsThe protein levels of WDR34 in hepatocellular carcinoma (HCC) tissues were examined by western blot and immunohistochemistry. The effects of WDR34 on the growth and migration of HCC cells were examined using MTT assay and Boyden chamber assay. The interaction between Frizzled and Dvl was evaluated by immunoprecipitation and GST pull-down assay.
resultsIn this study, we have shown that WDR34, the binding protein of Frizzled (Fz) activated beta-catenin/TCF signaling by enhancing the interaction between Fz and Dvl2. WDR34 was found to up-regulate in HCC tissues, and its expression was negatively correlated with the survival of HCC patients. WDR34 promoted the growth, colony formation and migration of HCC cells. However, knocking down the expression of WDR34 inhibited the growth, colony formation and migration of HCC cells.
conclusionTaken together, this study demonstrated the oncogenic roles of WDR34 in the progression of HCC and suggested that WDR34 might be a therapeutic target for HCC.
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