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@ARTICLE{Duman:143679,
      author       = {A. C. Duman$^*$ and K. Yaqubi$^*$ and A. Hoffmann and A. A.
                      Acikgöz$^*$ and A. Korshunov and M. Bendszus and C.
                      Herold-Mende and H.-K. Liu$^*$ and J. Alfonso$^*$},
      title        = {{A}cyl-{C}o{A}-{B}inding {P}rotein {D}rives {G}lioblastoma
                      {T}umorigenesis by {S}ustaining {F}atty {A}cid {O}xidation.},
      journal      = {Cell metabolism},
      volume       = {30},
      number       = {2},
      issn         = {1550-4131},
      address      = {Cambridge, Mass.},
      publisher    = {Cell Press},
      reportid     = {DKFZ-2019-01253},
      pages        = {274-289.e5},
      year         = {2019},
      abstract     = {Glioblastoma multiforme (GBM) undergoes metabolic
                      reprogramming to meet the high ATP and anabolic demands of
                      the tumor cells. However, the role of fatty acid oxidation
                      (FAO) and its regulators in the GBM context has been largely
                      unknown. Here, we show that the neural stem cell
                      pro-proliferative factor acyl-CoA-binding protein (ACBP,
                      also known as DBI) is highly expressed in GBM, and by
                      binding to acyl-CoAs, it cell-autonomously maintains high
                      proliferation rates, promoting tumor growth and poor
                      survival in several preclinical models. Mechanistic
                      experiments using ACBP-acyl-CoA binding affinity variants
                      and pharmacological FAO modulators suggest that ACBP
                      supports tumor growth by controlling the availability of
                      long-chain fatty acyl-CoAs to mitochondria, promoting FAO in
                      GBM. Thus, our findings uncover a critical link between
                      lipid metabolism and GBM progression established by ACBP and
                      offer a potential therapeutic strategy for an effective
                      anti-proliferative metabolic management of GBM.},
      cin          = {A231 / A230 / A240},
      ddc          = {570},
      cid          = {I:(DE-He78)A231-20160331 / I:(DE-He78)A230-20160331 /
                      I:(DE-He78)A240-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31056285},
      doi          = {10.1016/j.cmet.2019.04.004},
      url          = {https://inrepo02.dkfz.de/record/143679},
}