Rare Diseases Symptoms Automatic Extraction
Home
A random Abstract
Our Project
Our Team
WIP is necessary for matrix invasion by breast cancer cells.
[wiskott-aldrich syndrome]
Actin
filament
assembly
and
reorganisation
during
cell
migration
and
invasion
into
extracellular
matrices
is
a
well-documented
phenomenon
.
Among
actin-binding
proteins
regulating
its
polymerisation
,
the
members
of
the
WASP
(
Wiskott
Aldrich
Syndrome
Protein
)
family
are
generally
thought
to
play
the
most
significant
role
in
supporting
cell
invasiveness
.
In
situ
,
cytosolic
N-WASP
(
neural
WASP
)
is
associated
with
a
partner
protein
termed
WIP
(
WASP
Interacting
Protein
)
that
is
bound
to
the
N-
terminal
domain
of
N-WASP
.
Despite
much
effort
,
rather
little
is
known
about
the
role
of
WIP
in
regulating
N-WASP
and
consequent
actin-filament
assembly
.
Even
less
is
known
about
the
function
of
WIP
within
the
specialised
cell
adhesion
and
attachment
structures
known
as
podosomes
and
invadopodia
.
In
particular
,
whilst
the
interaction
of
WIP
with
known
participants
in
the
development
and
maturation
of
invadopodia
such
as
N-WASP
,
the
Arp
2
/
3
complex
and
cortactin
has
been
described
,
little
is
known
concerning
the
direct
contribution
of
WIP
to
invadopodia
and
its
potential
role
as
a
regulator
of
cancer
cell
invasion
.
In
this
report
,
we
use
2
D
and
3
D
culture
systems
to
describe
the
role
played
by
WIP
in
modulating
the
morphology
and
invasiveness
of
metastatic
breast
cancer
cells
in
vitro
,
as
well
as
its
effect
on
the
process
of
mesenchymal-epithelial
transition
(
MET
)
seen
in
these
cells
.
We
demonstrate
that
WIP
is
necessary
for
invadopodium
formation
and
matrix
degradation
by
basal
breast
cancer
cells
,
but
not
sufficient
to
induce
invasiveness
in
luminal
cells
.
