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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},
}