ArticleHepatology (Baltimore, Md.)2013
Disordered purinergic signaling and abnormal cellular metabolism are associated with development of liver cancer in Cd39/ENTPD1 null mice.
Article in Hepatology (Baltimore, Md.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 86 citations in OpenAlex.
- Purinergic signal transduction and metabolic regulation by ENTPD5 and ENTPD6.Frontiers in endocrinology · 2026Review
- Purinergic pathways and their clinical use in the treatment of acute myeloid leukemia.Purinergic signalling · 2025Review
- Antisense to human CD39 dysregulates immune metabolism in inflammatory bowel disease.Cellular & molecular immunology · 2025Article
- Autophagic regulation of CD8Frontiers in cellular and infection microbiology · 2025Article
- Characterization of an Activated Metabolic Transcriptional Program in Hepatoblastoma Tumor Cells Using scRNA-seq.International journal of molecular sciences · 2024Article
- Beta vulgaris L. beetroot protects against iron-induced liver injury by restoring antioxidant pathways and regulating cellular functions.Scientific reports · 2024Article
- Platelets induce CD39 expression in tumor cells to facilitate tumor metastasis.British journal of cancer · 2024Article
- CD39American journal of cancer research · 2024Article
- Regulatory role of CD39 and CD73 in tumor immunity.Future oncology (London, England) · 2024Review
- Adenosine A2A receptor is a tumor suppressor of NASH-associated hepatocellular carcinoma.Cell reports. Medicine · 2023Article
- Review immune response of targeting CD39 in cancer.Biomarker research · 2023Review
- Blockade of PGK1 and ALDOA enhances bilirubin control of Th17 cells in Crohn's disease.Communications biology · 2022Article
- ATP and Adenosine Metabolism in Cancer: Exploitation for Therapeutic Gain.Pharmacological reviews · 2022Review
- Glioma Stem Cells Upregulate CD39 Expression to Escape Immune Response through SOX2 Modulation.Cancers · 2022Article
- Efficient recovery of potent tumour-infiltrating lymphocytes through quantitative immunomagnetic cell sorting.Nature biomedical engineering · 2022Article
- ENTPD1/CD39 as a predictive marker of treatment response to gemogenovatucel-T as maintenance therapy in newly diagnosed ovarian cancer.Communications medicine · 2022Article
- Emerging roles of purinergic signaling in anti-cancer therapy resistance.Frontiers in cell and developmental biology · 2022Review
- Extracellular vesicles and immunogenic stress in cancer.Cell death & disease · 2021Review
- CD39 Regulation and Functions in T Cells.International journal of molecular sciences · 2021Review
- Targeting ectonucleotidases to treat inflammation and halt cancer development in the gut.Biochemical pharmacology · 2021Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
unlabelledLiver cancer is associated with chronic inflammation, which is linked to immune dysregulation, disordered metabolism, and aberrant cell proliferation. Nucleoside triphosphate diphosphohydrolase-1; (CD39/ENTPD1) is an ectonucleotidase that regulates extracellular nucleotide/nucleoside concentrations by scavenging nucleotides to ultimately generate adenosine. These properties inhibit antitumor immune responses and promote angiogenesis, being permissive for the growth of transplanted tumors. Here we show that Cd39 deletion promotes development of both induced and spontaneous autochthonous liver cancer in mice. Loss of Cd39 results in higher concentrations of extracellular nucleotides, which stimulate proliferation of hepatocytes, abrogate autophagy, and disrupt glycolytic metabolism. Constitutive activation of Ras-mitogen-activated protein kinase (MAPK) and mammalian target of rapamycin (mTOR)-S6K1 pathways occurs in both quiescent Cd39 null hepatocytes in vitro and liver tissues in vivo. Exogenous adenosine 5'-triphosphate (ATP) boosts these signaling pathways, whereas rapamycin inhibits such aberrant responses in hepatocytes.
conclusionDeletion of Cd39 and resulting changes in disordered purinergic signaling perturb hepatocellular metabolic/proliferative responses, paradoxically resulting in malignant transformation. These findings might impact adjunctive therapies for cancer. Our studies indicate that the biology of autochthonous and transplanted tumors is quite distinct.
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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.