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@ARTICLE{Ashry:277877,
      author       = {R. Ashry and A. M. Mustafa and K. Hausmann and M.
                      Linnebacher and S. Strand and W. Sippl and M. Wirth$^*$ and
                      O. H. Krämer},
      title        = {{NOXA} {A}ccentuates {A}poptosis {I}nduction by a {N}ovel
                      {H}istone {D}eacetylase {I}nhibitor.},
      journal      = {Cancers},
      volume       = {15},
      number       = {14},
      issn         = {2072-6694},
      address      = {Basel},
      publisher    = {MDPI},
      reportid     = {DKFZ-2023-01545},
      pages        = {3650},
      year         = {2023},
      abstract     = {Epigenetic modifiers of the histone deacetylase (HDAC)
                      family are often dysregulated in cancer cells. Experiments
                      with small molecule HDAC inhibitors (HDACi) have proven that
                      HDACs are a vulnerability of transformed cells. We evaluated
                      a novel hydroxamic acid-based HDACi (KH16; termed yanostat)
                      in human pancreatic ductal adenocarcinoma (PDAC) cells,
                      short- and long-term cultured colorectal cancer (CRC) cells,
                      and retinal pigment epithelial cells. We show that KH16
                      induces cell cycle arrest and apoptosis, both time and dose
                      dependently in PDAC and CRC cells. This is associated with
                      altered expression of BCL2 family members controlling
                      intrinsic apoptosis. Recent data illustrate that PDAC cells
                      frequently have an altered expression of the pro-apoptotic
                      BH3-only protein NOXA and that HDACi induce an accumulation
                      of NOXA. Using PDAC cells with a deletion of NOXA by
                      CRISPR-Cas9, we found that a lack of NOXA delayed apoptosis
                      induction by KH16. These results suggest that KH16 is a new
                      chemotype of hydroxamic acid HDACi with superior activity
                      against solid tumor-derived cells. Thus, KH16 is a scaffold
                      for future research on compounds with nanomolar activity
                      against HDACs.},
      keywords     = {HDAC (Other) / HDACi (Other) / NOXA (Other) / apoptosis
                      (Other) / colon cancer (Other) / pancreatic cancer (Other)},
      cin          = {BE01},
      ddc          = {610},
      cid          = {I:(DE-He78)BE01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37509312},
      pmc          = {pmc:PMC10377841},
      doi          = {10.3390/cancers15143650},
      url          = {https://inrepo02.dkfz.de/record/277877},
}