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Upregulated WAVE3 expression is essential for TGF-β-mediated EMT and metastasis of triple-negative breast cancer cells.
[wiskott-aldrich syndrome]
Breast
cancer
is
the
second
leading
cause
of
cancer
death
in
women
in
the
United
States
.
Metastasis
accounts
for
the
death
of
~
90
%
of
these
patients
,
yet
the
mechanisms
underlying
this
event
remain
poorly
defined
.
WAVE
3
belongs
to
the
WASP
/
WAVE
family
of
actin-binding
proteins
that
play
essential
roles
in
regulating
cell
morphology
,
actin
polymerization
,
cytoskeleton
remodeling
,
cell
motility
,
and
invasion
.
Accordingly
,
we
demonstrated
previously
that
WAVE
3
promotes
the
acquisition
of
invasive
and
metastatic
phenotypes
by
human
breast
cancers
.
Herein
,
we
show
that
transforming
growth
factor
-β
(
TGF-β
)
selectively
and
robustly
induced
the
expression
of
WAVE
3
in
metastatic
breast
cancer
cells
,
but
not
in
their
nonmetastatic
counterparts
.
Moreover
,
the
induction
of
WAVE
3
expression
in
human
and
mouse
triple-negative
breast
cancer
cells
(
TNBCs
)
by
TGF-β
likely
reflects
its
coupling
to
microRNA
expression
via
a
Smad
2
-
and
β
3
integrin-dependent
mechanism
.
We
further
demonstrate
the
requirement
for
WAVE
3
expression
in
mediating
the
initiation
of
epithelial-mesenchymal
transition
(
EMT
)
programs
stimulated
by
TGF-β
.
Indeed
,
stable
depletion
of
WAVE
3
expression
in
human
TNBC
cells
prevented
TGF-β
from
inducing
EMT
programs
and
from
stimulating
the
proliferation
,
migration
,
and
the
formation
of
lamellipodia
in
metastatic
TNBC
cells
.
Lastly
,
we
observed
WAVE
3
deficiency
to
abrogate
the
outgrowth
of
TNBC
cell
organoids
in
3
-
dimensional
organotypic
cultures
as
well
as
to
decrease
the
growth
and
metastasis
of
4
T
1
tumors
produced
in
syngeneic
Balb
/
C
mice
.
Indeed
,
WAVE
3
deficiency
significantly
reduced
the
presence
of
sarcomatoid
morphologies
indicative
of
EMT
phenotypes
in
pulmonary
TNBC
tumors
as
compared
to
those
detected
in
their
parental
counterparts
.
Collectively
,
these
findings
indicate
the
necessity
for
WAVE
3
expression
and
activity
during
EMT
programs
stimulated
by
TGF-β
;
they
also
suggest
that
measures
capable
of
inactivating
WAVE
3
may
play
a
role
in
alleviating
metastasis
stimulated
by
TGF-β
.
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