ArticleInternational journal of biological sciences2022
Pantothenate Kinase 1 Inhibits the Progression of Hepatocellular Carcinoma by Negatively Regulating Wnt/β-catenin Signaling.
Article in International journal of biological sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Palmitoylation-related gene signature for immune subtyping, prognostic stratification, and immunotherapy guidance in hepatocellular carcinoma.Translational cancer research · 2026Article
- Astragalus Polysaccharides Target the Wnt/β-catenin Pathway to Suppress Malignant Behavior in Hepatocellular Carcinoma.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2026Article
- Exploration of signature-related FAM genes and correlation between FAM50A expression and the pathogenesis and prognosis of hepatocellular carcinoma.Translational cancer research · 2025Article
- Advances in Inflammatory Bowel Disease Diagnostics: Machine Learning and Genomic Profiling Reveal Key Biomarkers for Early Detection.Diagnostics (Basel, Switzerland) · 2024Article
- The Carcinogenic Potential of Bisphenol A in the Liver Based on Transcriptomic Studies.Cancers · 2023Article
- Article
- CSTF2 Acts as a Prognostic Marker Correlated with Immune Infiltration in Hepatocellular Carcinoma.Cancer management and research · 2022Article
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Authors and funding
22 authors at 8 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperactivation of Wnt/β-catenin signaling has been reported in hepatocellular carcinoma (HCC). However, the mechanisms underlying the hyperactivation of Wnt/β-catenin signaling are incompletely understood. In this study, Pantothenate kinase 1 (PANK1) is shown to be a negative regulator of Wnt/β-catenin signaling. Downregulation of PANK1 in HCC correlates with clinical features. Knockdown of PANK1 promotes the proliferation, growth and invasion of HCC cells, while overexpression of PANK1 inhibits the proliferation, growth, invasion and tumorigenicity of HCC cells. Mechanistically, PANK1 binds to CK1α, exerts protein kinase activity and cooperates with CK1α to phosphorylate N-terminal serine and threonine residues in β-catenin both in vitro and in vivo. Additionally, the expression levels of PANK1 and β-catenin can be used to predict the prognosis of HCC. Collectively, the results of this study highlight the crucial roles of PANK1 protein kinase activity in inhibiting Wnt/β-catenin signaling, suggesting that PANK1 is a potential therapeutic target for HCC.
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