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@ARTICLE{FahimGolestaneh:141806,
author = {A. Fahim Golestaneh$^*$ and L. S. M. Lecker$^*$ and J.
Schlegel$^*$ and A. Nowrouzi$^*$ and C. Schwager$^*$ and S.
Meister$^*$ and W. Weichert$^*$ and J. Debus$^*$ and A.
Abdollahi$^*$},
title = {{L}arge scale in-vivo micro-{RNA} loss of function screen
identified mi{R}-29a, mi{R}-100 and mi{R}-155 as modulators
of radioresistance and tumor-stroma communication.},
journal = {International journal of cancer},
volume = {144},
number = {11},
issn = {0020-7136},
address = {Bognor Regis},
publisher = {Wiley-Liss},
reportid = {DKFZ-2018-02074},
pages = {2774-2781},
year = {2019},
abstract = {Micro RNAs (miR) are master regulators of cellular
transcriptome. We aimed to investigate the role of miR
regulation on tumor radiosensitivity and development of
local tumor recurrence by a novel large-scale in-vivo loss
of function screen. For stable miR silencing, human A431
tumor cells were transduced with lentiviral constructs
against 170 validated human miR (miRzip library).
Fractionated radiotherapy (5x6Gy) was applied to A431 miRzip
library growing s.c. in NCr nude mice. Enrichment of miRZip
and miR expression was assessed using multiplexed qRT-PCR.
The modulatory effect of miR on tumor and tumor
microenvironment response to ionizing radiation was further
evaluated by clonogenic survival, apoptosis (Caspase 3/7),
DNA double-strand breaks (DSB, nuclear γH2AX foci), tumor
microvessel density (MVD), transcriptome and protein
analysis. Fractionated irradiation of the A431 miRzip
library led to regression of tumors. However, after a
latency period, tumors ultimately progressed and formed
local recurrences indicating the survival of a subpopulation
of miRzip expressing tumor clones. Among the selected miR
for subsequent validation studies, loss of miR-29a, miR-100
and miR-155 was found to enhance clonogenic survival, reduce
apoptosis and residual γH2AX foci of irradiated tumor
cells. Moreover, knockdown of miR increased tumor
angiogenesis correlating with elevated VEGF and TGFα
expression levels. This phenomenon was most evident after
tumor irradiation in-vivo suggesting a critical role for
tumor-stroma communication in development of the
radioresistant phenotype. Engineering radioresistant tumors
in-vivo by modulating miR expression may lead to
identification of critical targets for conquering local
therapy failure. This article is protected by copyright. All
rights reserved.},
cin = {E210 / E050 / L101},
ddc = {610},
cid = {I:(DE-He78)E210-20160331 / I:(DE-He78)E050-20160331 /
I:(DE-He78)L101-20160331},
pnm = {315 - Imaging and radiooncology (POF3-315)},
pid = {G:(DE-HGF)POF3-315},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:30478850},
doi = {10.1002/ijc.32019},
url = {https://inrepo02.dkfz.de/record/141806},
}