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@ARTICLE{Bayer:303494,
author = {M. Bayer and J. Zajakina and M. Schäfer and K. Salmina and
F. Rumnieks and J. Jansons and F. Bestvater$^*$ and R. Kurg
and J. Erenpreisa and M. Hausmann},
title = {{C}hemotherapy ({E}toposide)-{I}nduced {I}ntermingling of
{H}eterochromatin and {E}uchromatin {C}ompartments in
{S}enescent {PA}-1 {E}mbryonal {C}arcinoma {C}ells.},
journal = {Cancers},
volume = {17},
number = {15},
issn = {2072-6694},
address = {Basel},
publisher = {MDPI},
reportid = {DKFZ-2025-01685},
pages = {2480},
year = {2025},
abstract = {Background: Often, neoadjuvant therapy, which relies on the
induction of double-strand breaks (DSBs), is used prior to
surgery to shrink tumors by inducing cancer cell apoptosis.
However, recent studies have suggested that this treatment
may also induce a fluctuating state between senescence and
stemness in PA-1 embryonal carcinoma cells, potentially
affecting therapeutic outcomes. Thus, the respective
epigenetic pathways are up or downregulated over a time
period of days. These fluctuations go hand in hand with
changes in spatial DNA organization. Methods: By means of
Single-Molecule Localization Microscopy in combination with
mathematical evaluation tools for pointillist data sets, we
investigated the organization of euchromatin and
heterochromatin at the nanoscale on the third and fifth day
after etoposide treatment. Results: Using fluorescently
labeled antibodies against H3K9me3 (heterochromatin
tri-methylation sites) and H3K4me3 (euchromatin
tri-methylation sites), we found that the induction of DSBs
led to the de-condensation of heterochromatin and compaction
of euchromatin, with a peak effect on day 3 after the
treatment. On day 3, we also observed the co-localization of
euchromatin and heterochromatin, which have marks that
usually occur in exclusive low-overlapping network-like
compartments. The evaluation of the SMLM data using
topological tools (persistent homology and persistent
imaging) and principal component analysis, as well as the
confocal microscopy analysis of H3K9me3- and H3K4me3-stained
PA-1 cells, supported the findings that distinct shifts in
euchromatin and heterochromatin organization took place in a
subpopulation of these cells during the days after the
treatment. Furthermore, by means of flow cytometry, it was
shown that the rearrangements in chromatin organization
coincided with the simultaneous upregulation of the stemness
promotors OCT4A and SOX2 and senescence promotors p21Cip1
and p27. Conclusions: Our findings suggest potential
applications to improve cancer therapy by inhibiting
chromatin remodeling and preventing therapy-induced
senescence.},
keywords = {DNA damage by etoposide (Other) / cell-fate (Other) /
chromatin re-organization in tumor cells (Other) /
senescence (Other) / single-molecule localization microscopy
(Other) / statistical and topological data evaluation
(Other) / stemness self-renewal (Other)},
cin = {W210},
ddc = {610},
cid = {I:(DE-He78)W210-20160331},
pnm = {319H - Addenda (POF4-319H)},
pid = {G:(DE-HGF)POF4-319H},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:40805179},
doi = {10.3390/cancers17152480},
url = {https://inrepo02.dkfz.de/record/303494},
}