ArticleCellular and molecular gastroenterology and hepatology2018
Gankyrin Promotes Tumor-Suppressor Protein Degradation to Drive Hepatocyte Proliferation.
Article in Cellular and molecular gastroenterology and hepatology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Structural modification of the propyl linker of cjoc42 in combination with sulfonate ester and triazole replacements for enhanced gankyrin binding and anti-proliferative activity.Bioorganic & medicinal chemistry · 2024Article
- Synthesis and evaluation of 2,5-substituted pyrimidines as small-molecule gankyrin binders.Future medicinal chemistry · 2024Article
- Small-Molecule Gankyrin Inhibition as a Therapeutic Strategy for Breast and Lung Cancer.Journal of medicinal chemistry · 2022Article
- Second Generation Small Molecule Inhibitors of Gankyrin for the Treatment of Pediatric Liver Cancer.Cancers · 2022Article
- Small Molecule Cjoc42 Improves Chemo-Sensitivity and Increases Levels of Tumor Suppressor Proteins in Hepatoblastoma Cells and in Mice by Inhibiting Oncogene Gankyrin.Frontiers in pharmacology · 2021Article
- Liver Proliferation Is an Essential Driver of Fibrosis in Mouse Models of Nonalcoholic Fatty Liver Disease.Hepatology communications · 2019Article
- Small-Molecule Inhibitors of the Proteasome's Regulatory Particle.Chembiochem : a European journal of chemical biology · 2019Review
- Tumor Suppressor Down-Regulation Promotes Hepatocyte Proliferation: A New GANKster on the Block.Cellular and molecular gastroenterology and hepatology · 2018Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Background & Aims: Uncontrolled liver proliferation is a key characteristic of liver cancer; however, the mechanisms by which this occurs are not well understood. Elucidation of these mechanisms is necessary for the development of better therapy. The oncogene Gankyrin (Gank) is overexpressed in both hepatocellular carcinoma and hepatoblastoma. The aim of this work was to determine the role of Gank in liver proliferation and elucidate the mechanism by which Gank promotes liver proliferation. Methods: We generated Gank liver-specific knock-out (GLKO) mice and examined liver biology and proliferation after surgical resection and liver injury. Results: Global profiling of gene expression in GLKO mice showed significant changes in pathways involved in liver cancer and proliferation. Investigations of liver proliferation after partial hepatectomy and CCl Conclusions: These studies show that Gank promotes hepatocyte proliferation by elimination of TSPs. This work provides background for the development of Gank-mediated therapy for the treatment of liver cancer. RNA sequencing data can be accessed in the NCBI Gene Expression Omnibus: GSE104395.
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Registered trials
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