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@ARTICLE{Vallet:130705,
author = {S. Vallet and M. H. Bashari and F.-J. Fan and S. Malvestiti
and A. Schneeweiss and P. Wuchter and D. Jäger$^*$ and K.
Podar$^*$},
title = {{P}re-{O}steoblasts {S}timulate {M}igration of {B}reast
{C}ancer {C}ells via the {HGF}/{MET} {P}athway.},
journal = {PLoS one},
volume = {11},
number = {3},
issn = {1932-6203},
address = {Lawrence, Kan.},
publisher = {PLoS},
reportid = {DKFZ-2017-05783},
pages = {e0150507 -},
year = {2016},
abstract = {The occurrence of skeletal metastases in cancer, e.g.
breast cancer (BC), deteriorates patient life expectancy and
quality-of-life. Current treatment options against
tumor-associated bone disease are limited to anti-resorptive
therapies and aimed towards palliation. There remains a lack
of therapeutic approaches, which reverse or even prevent the
development of bone metastases. Recent studies demonstrate
that not only osteoclasts (OCs), but also osteoblasts (OBs)
play a central role in the pathogenesis of skeletal
metastases, partly by producing hepatocyte growth factor
(HGF), which promotes tumor cell migration and seeding into
the bone. OBs consist of a heterogeneous cell pool with
respect to their maturation stage and function. Recent
studies highlight the critical role of pre-OBs in
hematopoiesis. Whether the development of bone metastases
can be attributed to a particular OB maturation stage is
currently unknown.Pre-OBs were generated from healthy donor
(HD)-derived bone marrow stromal cells (BMSC) as well as the
BMSC line KM105 and defined as ALPlow OPNlow RUNX2high OSX
high CD166high. Conditioned media (CM) of pre-OBs, but not
of undifferentiated cells or mature OBs, enhanced migration
of metastatic BC cells. Importantly, HGF mRNA was
significantly up-regulated in pre-OBs versus mature OBs, and
CM of pre-OBs activated the MET signaling pathway.
Highlighting a key role for HGF, CM from HGF-negative
pre-OBs derived from the BMSC line HS27A did not support
migration of BC cells. Genetically (siMET) or
pharmacologically (INCB28060) targeting MET inhibited both
HGF- and pre-OB CM- mediated BC cell migration.Our data
demonstrate for the first time a role for pre-OBs in
mediating HGF/MET- dependent migration of BC cells and
strongly support the clinical evaluation of INCB28060 and
other MET inhibitors to limit and/or prevent BC-associated
bone metastases.},
keywords = {2-fluoro-N-methyl-4-(7-(quinolin-6-yl-methyl)imidazo(1,2-b)(1,2,4)triazin-2-yl)benzamide
(NLM Chemicals) / Benzamides (NLM Chemicals) / Bridged
Bicyclo Compounds, Heterocyclic (NLM Chemicals) / Culture
Media, Conditioned (NLM Chemicals) / HGF protein, human (NLM
Chemicals) / RNA, Small Interfering (NLM Chemicals) /
Hepatocyte Growth Factor (NLM Chemicals) / MET protein,
human (NLM Chemicals) / Proto-Oncogene Proteins c-met (NLM
Chemicals)},
cin = {G010 / D120},
ddc = {500},
cid = {I:(DE-He78)G010-20160331 / I:(DE-He78)D120-20160331},
pnm = {314 - Tumor immunology (POF3-314)},
pid = {G:(DE-HGF)POF3-314},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:26934743},
pmc = {pmc:PMC4774929},
doi = {10.1371/journal.pone.0150507},
url = {https://inrepo02.dkfz.de/record/130705},
}