ArticleProceedings of the National Academy of Sciences of the United States of America2011
Depletion of β-catenin from mature hepatocytes of mice promotes expansion of hepatic progenitor cells and tumor development.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- Article
- Loss of β-catenin reveals a role for glutathione in regulating oxidative stress during cholestatic liver disease.Hepatology communications · 2024Article
- Unique Features of Hepatitis B Virus-Related Hepatocellular Carcinoma in Pathogenesis and Clinical Significance.Cancers · 2021Review
- Inhibition of β-Catenin Activity Abolishes LKB1 Loss-Driven Pancreatic Cystadenoma in Mice.International journal of molecular sciences · 2021Article
- Complement C1q mediates the expansion of periportal hepatic progenitor cells in senescence-associated inflammatory liver.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- BRG1 Mediates Nephronectin Activation in Hepatocytes to Promote T Lymphocyte Infiltration in ConA-Induced Hepatitis.Frontiers in cell and developmental biology · 2020Article
- Loss of autophagy impairs physiological steatosis by accumulation of NCoR1.Life science alliance · 2020Article
- Hepatocyte-Specific β-Catenin Deletion During Severe Liver Injury Provokes Cholangiocytes to Differentiate Into Hepatocytes.Hepatology (Baltimore, Md.) · 2019Article
- Shp2 deletion in hepatocytes suppresses hepatocarcinogenesis driven by oncogenic β-Catenin, PIK3CA and MET.Journal of hepatology · 2018Article
- β2 spectrin-mediated differentiation repressed the properties of liver cancer stem cells through β-catenin.Cell death & disease · 2018Article
- Role of insulin receptor substrates in the progression of hepatocellular carcinoma.Scientific reports · 2017Article
- The potential role of liver stem cells in initiation of primary liver cancer.Hepatology international · 2016Review
- Hepatic Loss of Borealin Impairs Postnatal Liver Development, Regeneration, and Hepatocarcinogenesis.The Journal of biological chemistry · 2016Article
- Double primary hepatic cancer (hepatocellular carcinoma and intrahepatic cholangiocarcinoma) originating from hepatic progenitor cell: a case report and review of the literature.World journal of surgical oncology · 2016Review
- Spontaneous development of hepatocellular carcinoma with cancer stem cell properties in PR-SET7-deficient livers.The EMBO journal · 2015Article
- Deletion of Wntless in myeloid cells exacerbates liver fibrosis and the ductular reaction in chronic liver injury.Fibrogenesis & tissue repair · 2015Article
- Proteasome dysfunction activates autophagy and the Keap1-Nrf2 pathway.The Journal of biological chemistry · 2014Article
- Expansion of hepatic stem cell compartment boosts liver regeneration.Stem cells and development · 2014Article
- A novel role of nucleostemin in maintaining the genome integrity of dividing hepatocytes during mouse liver development and regeneration.Hepatology (Baltimore, Md.) · 2013Article
- Over-expression of deubiquitinating enzyme USP14 in lung adenocarcinoma promotes proliferation through the accumulation of β-catenin.International journal of molecular sciences · 2013Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Depletion of β-catenin impairs regeneration of the rapid turn-over gut epithelial cells, but appears dispensable for that of the slow turn-over mature hepatocytes in mice until 1 y of age. As the life span of mature murine hepatocytes is about 400 d, we studied conditional β-catenin knockout mice (Alb-Cre;Ctnnb1(flx/flx)) until 20 mo of age to determine the function of β-catenin in the postnatal liver. β-catenin was absent from the hepatocytes of β-catenin knockout mice 4 wk after delivery. From 9 mo of age, hepatocytes were gradually replaced by newly formed β-catenin-positive hepatocytes, which constituted about 90% of hepatocytes at 18-20 mo of age. This process was accompanied by active proliferation of bile duct/ductule cells. β-catenin-positive hepatocytes exhibited elevated proliferation activity and expression of progenitor cell markers, but lower albumin and Cre. This might explain their intact β-catenin protein, and suggest their origins from hepatic progenitor cells. Liver tumors arose spontaneously from β-catenin-positive cells, and tumorigenesis was accelerated by hepatitis B X protein. These results indicate β-catenin critical for the regeneration of mature hepatocytes. Failure to regenerate mature hepatocytes results in proliferation of hepatic progenitor cells that are able to maintain liver function but are predisposed to form liver tumors.
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