ArticleJournal of the American Society of Nephrology : JASN2015
β-catenin links von Hippel-Lindau to aurora kinase A and loss of primary cilia in renal cell carcinoma.
Article in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 76 citations in OpenAlex.
- Recent advances in etiology and treatment of von Hippel-Lindau Disease (VHLD).Cancer metastasis reviews · 2026Review
- Checkpoint kinase 2 coordinates autophagy activation and Aurora kinase A degradation to regulate primary cilia for cell invasion.Cell communication and signaling : CCS · 2026Article
- Essential genetic mutations impair DNA damage repair and modulate tumor immune microenvironment in ccRCC.MedScience · 2026Review
- Primary cilia in cancer: structures, functions, mechanisms, and therapeutic implications.Cancer biology & medicine · 2025Review
- Hedgehog pathway, cell cycle, and primary cilium.Cell death discovery · 2025Review
- Histone Deacetylase 6 (HDAC6) in Ciliopathies: Emerging Insights and Therapeutic Implications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Association of the combined parameters including the frequency of primary cilia, PD-L1, Smoothened protein, membranous β-catenin and cytoplasmic β-catenin expression with the outcome of patients with clear cell renal cell carcinoma.Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia · 2025Article
- Review
- NAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The Role of HDAC6 in Glioblastoma Multiforme: A New Avenue to Therapeutic Interventions?Biomedicines · 2024Review
- Inhibition of primary cilia-hedgehog signaling axis triggers autophagic cell death and suppresses malignant progression of VHL wild-type ccRCC.Cell death & disease · 2024Article
- The significant others of aurora kinase a in cancer: combination is the key.Biomarker research · 2024Review
- Targeted deletion of von-Hippel-Lindau in the proximal tubule conditions the kidney against early diabetic kidney disease.Cell death & disease · 2023Article
- Review
- STIL/AURKA axis promotes cell proliferation by influencing primary cilia formation in bladder cancer.Journal of translational medicine · 2023Article
- Patterns of Ciliation and Ciliary Signaling in Cancer.Reviews of physiology, biochemistry and pharmacology · 2023Review
- Primary cilia: a novel research approach to overcome anticancer drug resistance.Frontiers in molecular biosciences · 2023Review
- Recent advances in the understanding of cilia mechanisms and their applications as therapeutic targets.Frontiers in molecular biosciences · 2023Review
- IQGAP3 in clear cell renal cell carcinoma contributes to drug resistance and genome stability.PeerJ · 2022Article
- STIL Acts as an Oncogenetic Driver in a Primary Cilia-Dependent Manner in Human Cancer.Frontiers in cell and developmental biology · 2022Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
von Hippel-Lindau (VHL) gene mutations are associated with clear cell renal cell carcinoma (ccRCC). A hallmark of ccRCC is loss of the primary cilium. Loss of this key organelle in ccRCC is caused by loss of VHL and associated with increased Aurora kinase A (AURKA) and histone deacetylase 6 (HDAC6) activities, which drive disassembly of the primary cilium. However, the underlying mechanism by which VHL loss increases AURKA levels has not been clearly elucidated, although it has been suggested that hypoxia-inducible factor-1α (HIF-1α) mediates increased AURKA expression in VHL-null cells. By contrast, we found that elevated AURKA expression is not increased by HIF-1α, suggesting an alternate mechanism for AURKA dysregulation in VHL-null cells. We report here that AURKA expression is driven by β-catenin transcription in VHL-null cells. In a panel of RCC cell lines, we observed nuclear accumulation of β-catenin and increased AURKA signaling to HDAC6. Moreover, HIF-1α inhibited AURKA expression by inhibiting β-catenin transcription. VHL knockdown activated β-catenin and elevated AURKA expression, decreased primary cilia formation, and caused significant shortening of cilia length in cells that did form cilia. The β-catenin responsive transcription inhibitor iCRT14 reduced AURKA levels and rescued ciliary defects, inducing a significant increase in primary cilia formation in VHL-deficient cells. These data define a role for β-catenin in regulating AURKA and formation of primary cilia in the setting of VHL deficiency, opening new avenues for treatment with β-catenin inhibitors to rescue ciliogenesis in ccRCC.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.