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@ARTICLE{PierzynskaMach:278354,
      author       = {A. Pierzynska-Mach and I. Cainero and M. Oneto and E.
                      Ferrando-May$^*$ and L. Lanzanò and A. Diaspro},
      title        = {{I}maging-based study demonstrates how the {DEK} nanoscale
                      distribution differentially correlates with epigenetic marks
                      in a breast cancer model.},
      journal      = {Scientific reports},
      volume       = {13},
      number       = {1},
      issn         = {2045-2322},
      address      = {[London]},
      publisher    = {Macmillan Publishers Limited, part of Springer Nature},
      reportid     = {DKFZ-2023-01608},
      pages        = {12749},
      year         = {2023},
      abstract     = {Epigenetic dysregulation of chromatin is one of the
                      hallmarks of cancer development and progression, and it is
                      continuously investigated as a potential general bio-marker
                      of this complex disease. One of the nuclear factors involved
                      in gene regulation is the unique DEK protein-a histone
                      chaperon modulating chromatin topology. DEK expression
                      levels increase significantly from normal to cancer cells,
                      hence raising the possibility of using DEK as a tumor
                      marker. Although DEK is known to be implicated in epigenetic
                      and transcriptional regulation, the details of these
                      interactions and their relevance in cancer development
                      remain largely elusive. In this work, we investigated the
                      spatial correlation between the nuclear distribution of DEK
                      and chromatin patterns-alongside breast cancer
                      progression-leveraging image cross-correlation spectroscopy
                      (ICCS) coupled with Proximity Ligation Assay (PLA) analysis.
                      We performed our study on the model based on three
                      well-established human breast cell lines to consider this
                      tumor's heterogeneity (MCF10A, MCF7, and MDA-MB-231 cells).
                      Our results show that overexpression of DEK correlates with
                      the overall higher level of spatial proximity between DEK
                      and histone marks corresponding to gene promoters regions
                      (H3K9ac, H3K4me3), although it does not correlate with
                      spatial proximity between DEK and gene enhancers (H3K27ac).
                      Additionally, we observed that colocalizing fractions of DEK
                      and histone marks are lower for the non-invasive cell
                      subtype than for the highly invasive cell line (MDA-MB-231).
                      Thus, this study suggests that the role of DEK on
                      transcriptionally active chromatin regions varies depending
                      on the subtype of the breast cancer cell line.},
      cin          = {W650},
      ddc          = {600},
      cid          = {I:(DE-He78)W650-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37550322},
      doi          = {10.1038/s41598-023-38685-7},
      url          = {https://inrepo02.dkfz.de/record/278354},
}