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@ARTICLE{Tran:289597,
      author       = {C. S. Tran and J. Kersten and J. Yan and M. Breinig$^*$ and
                      T. Huth and T. Poth and O. Colasanti and T. Riedl$^*$ and S.
                      Faure-Dupuy and S. Diehl and L. Verhoye and T.-F. Li and M.
                      Lingemann and P. Schult and G. Ahlén and L. Frelin and F.
                      Kühnel and F. W. R. Vondran and K. Breuhahn and P. Meuleman
                      and M. Heikenwälder and P. Schirmacher and R.
                      Bartenschlager$^*$ and V. Laketa and S. Roessler and D. F.
                      Tschaharganeh$^*$ and M. Sällberg and V. Lohmann},
      title        = {{P}hosphatidylinositol 4-kinase {III} alpha governs
                      cytoskeletal organization for invasiveness of liver cancer
                      cells.},
      journal      = {Gastroenterology},
      volume       = {167},
      number       = {3},
      issn         = {0016-5085},
      address      = {Philadelphia, Pa. [u.a.]},
      publisher    = {Saunders},
      reportid     = {DKFZ-2024-00830},
      pages        = {522-537},
      year         = {2024},
      note         = {2024 Aug;167(3):522-537},
      abstract     = {High expression of phosphatidylinositol 4-kinase III alpha
                      (PI4KIIIα) correlates with poor survival rates in patients
                      with hepatocellular carcinoma (HCC). In addition, Hepatitis
                      C virus (HCV) infections activate PI4KIIIα and contribute
                      to HCC progression. We aimed at mechanistically
                      understanding the impact of PI4KIIIα on the progression of
                      liver cancer and the potential contribution of HCV in this
                      process.Several hepatic cell culture and mouse models were
                      used to study functional importance of PI4KIIIα on liver
                      pathogenesis. Antibody arrays, gene silencing and PI4KIIIα
                      specific inhibitor were applied to identify the involved
                      signaling pathways. The contribution of HCV was examined by
                      using HCV infection or overexpression of its nonstructural
                      protein.High PI4KIIIα expression and/or activity induced
                      cytoskeletal rearrangements via increased-phosphorylation of
                      paxillin and cofilin. This led to morphological alterations
                      and higher migratory and invasive properties of liver cancer
                      cells. We further identified the liver specific lipid kinase
                      phosphatidylinositol 3-kinase C2 domain-containing subunit
                      gamma (PIK3C2γ) working downstream of PI4KIIIα in
                      regulation of the cytoskeleton. PIK3C2γ generates plasma
                      membrane (PM) phosphatidylinositol 3,4-bisphosphate
                      [PI(3,4)P2]-enriched, invadopodia-like structures which
                      regulate cytoskeletal reorganization by promoting Akt2
                      phosphorylation.PI4KIIIα regulates cytoskeleton
                      organization via PIK3C2γ/Akt2/paxillin-cofilin to favor
                      migration and invasion of liver cancer cells. These findings
                      provide mechanistic insight into the contribution of
                      PI4KIIIα and HCV to progression of liver cancer and
                      identify promising targets for therapeutic intervention.},
      keywords     = {Akt2 (Other) / HCV (Other) / PIK3C2G (Other) /
                      hepatocellular carcinoma (Other) / phospholipid (Other)},
      cin          = {F190 / F180 / D440 / F170 / D430},
      ddc          = {610},
      cid          = {I:(DE-He78)F190-20160331 / I:(DE-He78)F180-20160331 /
                      I:(DE-He78)D440-20160331 / I:(DE-He78)F170-20160331 /
                      I:(DE-He78)D430-20160331},
      pnm          = {314 - Immunologie und Krebs (POF4-314)},
      pid          = {G:(DE-HGF)POF4-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38636680},
      doi          = {10.1053/j.gastro.2024.04.009},
      url          = {https://inrepo02.dkfz.de/record/289597},
}