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@ARTICLE{CidreAranaz:310292,
      author       = {F. Cidre-Aranaz$^*$ and F. H. Geyer$^*$ and T. Hölting$^*$
                      and K. M. Hanssen$^*$ and T. Faehling$^*$ and A. Ritter$^*$
                      and M. Zimmermann$^*$ and L. Mao$^*$ and J. Alonso and A.
                      Sastre and A. K. Jayavelu$^*$ and M. M. L. Knott$^*$ and J.
                      Musa$^*$ and T. Grünewald$^*$},
      title        = {c{IAP}1 inhibitor of apoptosis is a tumor suppressor in
                      {E}wing sarcoma.},
      journal      = {Cancer letters},
      volume       = {nn},
      issn         = {0304-3835},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier Science},
      reportid     = {DKFZ-2026-00515},
      pages        = {nn},
      year         = {2026},
      note         = {#EA:B410#LA:B410# / epub},
      abstract     = {Ewing sarcoma (EwS) is a highly aggressive pediatric
                      malignancy driven by EWSR1::ETS fusion oncoproteins
                      -primarily EWSR1::FLI1- which deregulate genes essential for
                      differentiation, proliferation, and cell survival. To
                      uncover key downstream targets of this fusion involved in
                      cell differentiation, we combined transcriptomic profiling
                      of EwS cell lines following EWSR1::FLI1 inhibition with gene
                      ontology analysis, a clinically annotated gene expression
                      dataset derived from EwS patient material and network
                      analyses. This integrative approach identified inhibitor of
                      apoptosis protein 1 (cIAP1, alias BIRC2) as an
                      EWSR1::FLI1-suppressed gene. Despite its known oncogenic
                      role in many cancers, cIAP1 showed minimal expression in
                      EwS. Using inducible cIAP1 re-expression models in EwS
                      cells, we demonstrated that cIAP1 re-expression suppresses
                      proliferation, clonogenic growth, and 3D spheroid formation
                      in vitro. Transcriptomic and proteomic analyses revealed
                      that low cIAP1 expression enhances proliferation-related
                      gene signatures, which are inhibited upon cIAP1
                      re-expression. In vivo xenograft models revealed that cIAP1
                      re-expression significantly reduces tumor growth, mitotic
                      activity, and Ki-67 positivity, while increasing tumor
                      necrosis and apoptosis. These findings highlight an
                      unexpected tumor-suppressive role for cIAP1 in fusion-driven
                      sarcomas, contrasting with its pro-survival function in
                      other cancers. Collectively, our results identify cIAP1 as a
                      prognostically relevant, EWSR1::FLI1-regulated hub whose
                      re-expression disrupts tumor progression, offering a
                      potential therapeutic strategy to restore tumor-suppressive
                      pathways in EwS.},
      keywords     = {BIRC2 (Other) / Ewing sarcoma (Other) / apoptosis (Other) /
                      cIAP1 (Other) / pediatric sarcoma (Other)},
      cin          = {B410 / HD01 / A400},
      ddc          = {570},
      cid          = {I:(DE-He78)B410-20160331 / I:(DE-He78)HD01-20160331 /
                      I:(DE-He78)A400-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41780845},
      doi          = {10.1016/j.canlet.2026.218389},
      url          = {https://inrepo02.dkfz.de/record/310292},
}