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@ARTICLE{Thier:275768,
      author       = {A. C. Thier$^*$ and B. Di Marco$^*$ and E. Nevedomskaya and
                      B. Ulug$^*$ and R. Lesche and S. Christian and J.
                      Alfonso$^*$},
      title        = {{T}argeting fatty acid oxidation via {A}cyl-{C}o{A} binding
                      protein hinders glioblastoma invasion.},
      journal      = {Cell death $\&$ disease},
      volume       = {14},
      number       = {4},
      issn         = {2041-4889},
      address      = {London [u.a.]},
      publisher    = {Nature Publishing Group},
      reportid     = {DKFZ-2023-00867},
      pages        = {296},
      year         = {2023},
      note         = {#EA:A230#LA:A230#},
      abstract     = {The diffuse nature of Glioblastoma (GBM) tumors poses a
                      challenge to current therapeutic options. We have previously
                      shown that Acyl-CoA Binding Protein (ACBP, also known as
                      DBI) regulates lipid metabolism in GBM cells, favoring fatty
                      acid oxidation (FAO). Here we show that ACBP downregulation
                      results in wide transcriptional changes affecting
                      invasion-related genes. In vivo experiments using
                      patient-derived xenografts combined with in vitro models
                      demonstrated that ACBP sustains GBM invasion via binding to
                      fatty acyl-CoAs. Blocking FAO mimics ACBPKD-induced
                      immobility, a cellular phenotype that can be rescued by
                      increasing FAO rates. Further investigation into
                      ACBP-downstream pathways served to identify Integrin beta-1,
                      a gene downregulated upon inhibition of either ACBP
                      expression or FAO rates, as a mediator for ACBP's role in
                      GBM invasion. Altogether, our findings highlight a role for
                      FAO in GBM invasion and reveal ACBP as a therapeutic
                      vulnerability to stall FAO and subsequent cell invasion in
                      GBM tumors.},
      keywords     = {Humans / Carrier Proteins: metabolism / Glioblastoma:
                      genetics / Diazepam Binding Inhibitor: metabolism / Lipid
                      Metabolism / Fatty Acids: metabolism / Carrier Proteins (NLM
                      Chemicals) / Diazepam Binding Inhibitor (NLM Chemicals) /
                      Fatty Acids (NLM Chemicals)},
      cin          = {A230},
      ddc          = {570},
      cid          = {I:(DE-He78)A230-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37120445},
      pmc          = {pmc:PMC10148872},
      doi          = {10.1038/s41419-023-05813-0},
      url          = {https://inrepo02.dkfz.de/record/275768},
}