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@ARTICLE{Wiedmann:275610,
      author       = {L. Wiedmann$^*$ and F. De Angelis Rigotti$^*$ and N.
                      Vaquero-Siguero$^*$ and E. Donato$^*$ and E. Espinet$^*$ and
                      I. Moll$^*$ and E. Alsina-Sanchis$^*$ and H. Bohnenberger
                      and E. Fernandez-Florido$^*$ and R. Mülfarth$^*$ and M.
                      Vacca$^*$ and J. Gerwing$^*$ and L.-C. Conradi and P.
                      Ströbel and A. Trumpp$^*$ and C. Mogler and A. Fischer$^*$
                      and J. Rodriguez-Vita$^*$},
      title        = {{HAPLN}1 potentiates peritoneal metastasis in pancreatic
                      cancer.},
      journal      = {Nature Communications},
      volume       = {14},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2023-00816},
      pages        = {2353},
      year         = {2023},
      note         = {#EA:A270#LA:A270#},
      abstract     = {Pancreatic ductal adenocarcinoma (PDAC) frequently
                      metastasizes into the peritoneum, which contributes to poor
                      prognosis. Metastatic spreading is promoted by cancer cell
                      plasticity, yet its regulation by the microenvironment is
                      incompletely understood. Here, we show that the presence of
                      hyaluronan and proteoglycan link protein-1 (HAPLN1) in the
                      extracellular matrix enhances tumor cell plasticity and PDAC
                      metastasis. Bioinformatic analysis showed that HAPLN1
                      expression is enriched in the basal PDAC subtype and
                      associated with worse overall patient survival. In a mouse
                      model for peritoneal carcinomatosis, HAPLN1-induced
                      immunomodulation favors a more permissive microenvironment,
                      which accelerates the peritoneal spread of tumor cells.
                      Mechanistically, HAPLN1, via upregulation of tumor necrosis
                      factor receptor 2 (TNFR2), promotes TNF-mediated
                      upregulation of Hyaluronan (HA) production, facilitating
                      EMT, stemness, invasion and immunomodulation. Extracellular
                      HAPLN1 modifies cancer cells and fibroblasts, rendering them
                      more immunomodulatory. As such, we identify HAPLN1 as a
                      prognostic marker and as a driver for peritoneal metastasis
                      in PDAC.},
      cin          = {A270 / A010},
      ddc          = {500},
      cid          = {I:(DE-He78)A270-20160331 / I:(DE-He78)A010-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37095087},
      doi          = {10.1038/s41467-023-38064-w},
      url          = {https://inrepo02.dkfz.de/record/275610},
}