% IMPORTANT: The following is UTF-8 encoded. This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.
@ARTICLE{Grnow:120527,
author = {J. Grünow$^*$ and C. Rong and J. Hischmann and K. Zaoui
and C. Flechtenmacher and K.-J. Weber and P. Plinkert and J.
Hess$^*$},
title = {{R}egulation of submaxillary gland androgen-regulated
protein 3{A} via estrogen receptor 2 in radioresistant head
and neck squamous cell carcinoma cells.},
journal = {Journal of experimental $\&$ clinical cancer research},
volume = {36},
number = {1},
issn = {1756-9966},
address = {Berlin},
publisher = {Springer},
reportid = {DKFZ-2017-00956},
pages = {25},
year = {2017},
abstract = {Molecular mechanisms of intrinsic or acquired
radioresistance serve as critical barrier for curative
therapy of head and neck squamous cell carcinoma (HNSCC) and
remain a major obstacle for progression-free and
disease-specific survival.HNSCC cell lines were treated with
a protocol of fractionated irradiation (IR, 4× 2Gy) alone
or in combination with antagonists of estrogen receptor
signaling and viability was determined by a colony-forming
assay (CFA). Expression of submaxillary gland
androgen-regulated protein 3A (SMR3A) and estrogen receptor
2 (ESR2) were assessed in tumor cells in vitro by RQ-PCR,
Western blot analysis and immunofluorescence staining, and
by immunohistochemical staining of tissue microarrays
containing tumor sections from patients with oropharyngeal
squamous cell carcinoma (OPSCC), which were treated by
definitive or adjuvant radiotherapy. Subgroups with distinct
SMR3A and ESR2 expression patterns were correlated with
clinical parameters and survival outcome including
multivariable analysis.Fractionated irradiation (IR)
revealed an accumulation of tumor cells with prominent SMR3A
expression, which was accompanied by an up-regulation of the
estrogen receptor 2 (ESR2). ESR2-dependent regulation of
SMR3A was supported by induced expression after stimulation
with estradiol (E2), which was impaired by co-treatment with
4-Hydroxytamoxifen (TAM) or Fulvestrant, respectively. Both
drugs significantly sensitized FaDu cells to fractionated IR
as determined by a CFA and accelerated apoptosis. These data
suggest a critical role of ESR2 in radioresistance and that
SMR3A might serve as a surrogate marker for active ESR2
signaling. In line with this assumption, ESR2-positive
oropharyngeal squamous cell carcinoma (OPSCC) with high
SMR3A expression had an unfavorable progression-free and
disease-specific survival as compared to those tumors with
low SMR3A expression.In summary, our findings provide
compelling experimental evidence that HNSCC with SMR3A and
ESR2 co-expression have a higher risk for treatment failure
and these patients might benefit from clinically
well-established drugs targeting estrogen receptor
signaling.},
cin = {G405},
ddc = {610},
cid = {I:(DE-He78)G405-20160331},
pnm = {317 - Translational cancer research (POF3-317)},
pid = {G:(DE-HGF)POF3-317},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:28166815},
pmc = {pmc:PMC5294868},
doi = {10.1186/s13046-017-0496-2},
url = {https://inrepo02.dkfz.de/record/120527},
}