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@ARTICLE{Huang:300266,
      author       = {J. C. Huang and X. L. Tong and M. S. W. Xiang and B. B.
                      Boumelhem and D. P. Foulis and M. Zhang and C. A. McKenzie
                      and G. W. McCaughan and T. Reinheckel$^*$ and H. E. Zhang
                      and M. D. Gorrell},
      title        = {{D}ipeptidyl peptidase 9 ({DPP}9) depletion from
                      hepatocytes in experimental primary liver cancer.},
      journal      = {Biochimica et biophysica acta / Molecular basis of disease},
      volume       = {1871},
      number       = {5},
      issn         = {0006-3002},
      address      = {Amsterdam},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2025-00719},
      pages        = {167819},
      year         = {2025},
      abstract     = {Dipeptidyl peptidase 9 (DPP9) is an indispensable
                      intracellular protease. Among its many molecular functions
                      is suppression of the NLRP1 inflammasome. Inhibitors
                      targeting all four proteases of the DPP4 family, including
                      DPP9, can reduce tumour burden, including in mouse liver. To
                      explore hepatocyte DPP9 in experimental hepatocellular
                      carcinoma (HCC), we generated hepatocyte-specific DPP9-KO
                      mice by crossing albumin-Cre mice with DPP9 floxed mice and
                      treated sequentially with diethylnitrosamine, then with
                      thioacetamide combined with an atherogenic high-fat diet
                      until 28 weeks of age. DPP9-KO mice had less body, liver and
                      subcutaneous adipose tissue mass, lower fasting plasma
                      glucose and fewer small macroscopic liver nodules compared
                      to DPP9-WT control mice. However, there were no differences
                      in the total number of macroscopic liver nodules, or of
                      microscopic tumour burden, inflammation, fibrosis or
                      steatosis. Consistent with the known function of DPP9 to
                      suppress NLRP1 activation, activated caspase-1 protein and
                      inflammation markers Nfkbib, Cxcl10 and Ccl5 were elevated
                      in DPP9-KO liver. The tumour suppressor protein p53 was
                      increased and the autophagy proteins beclin1, LC3B and p62
                      were altered. In conclusion, hepatocyte-specific DPP9 gene
                      deletion in experimental primary liver cancer improved
                      energy metabolism and may reduce liver cancer initiation,
                      via mechanisms that may include increased autophagy and
                      tumour suppression.},
      keywords     = {Adiposity (Other) / Autophagy (Other) / Dipeptidyl
                      peptidase 9 (Other) / Glucose homeostasis (Other) /
                      Hepatocellular carcinoma (Other) / Histopathology (Other) /
                      Inflammasome (Other) / Serine protease (Other) / tp53
                      (Other)},
      cin          = {FR01},
      ddc          = {610},
      cid          = {I:(DE-He78)FR01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40187163},
      doi          = {10.1016/j.bbadis.2025.167819},
      url          = {https://inrepo02.dkfz.de/record/300266},
}