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Characterization of cancer stem-like cells derived from mouse induced pluripotent stem cells transformed by tumor-derived extracellular vesicles.
[liposarcoma]
Several
studies
have
shown
that
cancer
niche
can
perform
an
active
role
in
the
regulation
of
tumor
cell
maintenance
and
progression
through
extracellular
vesicles-based
intercellular
communication
.
However
,
it
has
not
been
reported
whether
this
vesicle-mediated
communication
affects
the
malignant
transformation
of
normal
stem
cells
/
progenitors
.
We
have
previously
reported
that
the
conditioned
medium
derived
from
the
mouse
Lewis
Lung
Carcinoma
(
LLC
)
cell
line
can
convert
mouse
induced
pluripotent
stem
cells
(
miPSCs
)
into
cancer
stem
cells
(
CSCs
)
,
indicating
that
normal
stem
cells
when
placed
in
an
aberrant
microenvironment
can
give
rise
to
functionally
active
CSCs
.
Here
,
we
focused
on
the
contribution
of
tumor
-derived
extracellular
vesicles
(
tEVs
)
that
are
secreted
from
LLC
cells
to
induce
the
transformation
of
miPSCs
into
CSCs
.
We
isolated
tEVs
from
the
conditioned
medium
of
LLC
cells
,
and
then
the
differentiating
miPSCs
were
exposed
to
tEVs
for
4
weeks
.
The
resultant
tEV
treated
cells
(
miPS-LLCev
)
expressed
Nanog
and
Oct
3
/
4
proteins
comparable
to
miPSCs
.
The
frequency
of
sphere
formation
of
the
miPS-LLCev
cells
in
suspension
culture
indicated
that
the
self-renewal
capacity
of
the
miPS-LLCev
cells
was
significant
.
When
the
miPS-LLCev
cells
were
subcutaneously
transplanted
into
Balb
/
c
nude
mice
,
malignant
liposarcomas
with
extensive
angiogenesis
developed
.
miPS-LLCevPT
and
miPS-LLCevDT
,
the
cells
established
from
primary
site
and
disseminated
liposarcomas
,
respectively
,
showed
their
capacities
to
self-renew
and
differentiate
into
adipocytes
and
endothelial
cells
.
Moreover
,
we
confirmed
the
secondary
liposarcoma
development
when
these
cells
were
transplanted
.
Taken
together
,
these
results
indicate
that
miPS-LLCev
cells
possess
CSC
properties
.
Thus
,
our
current
study
provides
the
first
evidence
that
tEVs
have
the
potential
to
induce
CSC
properties
in
normal
tissue
stem
cells
/
progenitors
.
Diseases
Validation
Diseases presenting
"cancer"
symptom
achondroplasia
acute rheumatic fever
adrenal incidentaloma
alpha-thalassemia
benign recurrent intrahepatic cholestasis
cadasil
canavan disease
carcinoma of the gallbladder
cholangiocarcinoma
coats disease
congenital adrenal hyperplasia
congenital diaphragmatic hernia
cowden syndrome
cushing syndrome
cutaneous mastocytosis
dedifferentiated liposarcoma
dystrophic epidermolysis bullosa
epidermolysis bullosa simplex
erdheim-chester disease
erythropoietic protoporphyria
esophageal adenocarcinoma
esophageal carcinoma
esophageal squamous cell carcinoma
familial hypocalciuric hypercalcemia
familial mediterranean fever
gm1 gangliosidosis
heparin-induced thrombocytopenia
hereditary cerebral hemorrhage with amyloidosis
hirschsprung disease
hodgkin lymphoma, classical
inclusion body myositis
junctional epidermolysis bullosa
kabuki syndrome
kallmann syndrome
kindler syndrome
lamellar ichthyosis
liposarcoma
locked-in syndrome
lymphangioleiomyomatosis
monosomy 21
neuralgic amyotrophy
oculocutaneous albinism
oligodontia
oral submucous fibrosis
papillon-lefèvre syndrome
pendred syndrome
pleomorphic liposarcoma
primary effusion lymphoma
proteus syndrome
pyomyositis
pyruvate dehydrogenase deficiency
severe combined immunodeficiency
sneddon syndrome
systemic capillary leak syndrome
triple a syndrome
von hippel-lindau disease
waldenström macroglobulinemia
well-differentiated liposarcoma
werner syndrome
wiskott-aldrich syndrome
wolf-hirschhorn syndrome
x-linked adrenoleukodystrophy
This symptom has already been validated