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Laminin-332-integrin interaction: a target for cancer therapy?
[junctional epidermolysis bullosa]
For
many
years
,
extracellular
matrix
(
ECM
)
was
considered
to
function
as
a
tissue
support
and
filler
.
However
,
we
now
know
that
ECM
proteins
control
many
cellular
events
through
their
interaction
with
cell-surface
receptors
and
cytoplasmic
signaling
pathways
.
For
example
,
they
regulate
cell
proliferation
,
cell
division
,
cell
adhesion
,
cell
migration
,
and
apoptosis
.
We
focus
in
this
review
on
a
laminin
isoform
,
laminin-
332
(
formerly
termed
laminin-
5
)
,
a
major
component
of
the
basement
membrane
(
BM
)
of
skin
and
other
epithelial
tissues
.
It
is
composed
of
3
subunits
(
alpha
3
beta
3
and
gamma
3
and
interacts
with
at
least
two
integrin
receptors
expressed
by
epithelial
cells
(
alpha
3
beta
1
and
alpha
6
beta
4
integrin
.
Mutations
in
either
laminin-
332
or
integrin
alpha
6
beta
4
result
in
junctional
epidermolysis
bullosa
,
a
blistering
skin
disease
,
while
targeting
of
laminin-
332
by
autoantibodies
in
cicatricial
pemphigoid
leads
to
dysadhesion
of
epithelial
cells
from
their
underlying
connective
tissue
.
Abnormal
expression
of
laminin-
332
and
its
integrin
receptors
is
also
a
hallmark
of
certain
tumor
types
and
is
believed
to
promote
invasion
of
colon
,
breast
and
skin
cancer
cells
.
Moreover
,
there
is
emerging
evidence
that
laminin-
332
and
its
protease
degradation
products
are
not
only
found
at
the
leading
front
of
several
tumors
but
also
likely
induce
and
/
or
promote
tumor
cell
migration
.
Thus
,
in
this
review
,
we
focus
specifically
on
the
role
of
laminin-
332
and
its
integrin
receptors
in
adhesion
,
proliferation
,
and
migration
/
invasion
of
cancer
cells
.
Finally
,
we
discuss
strategies
for
the
development
of
laminin-
332
-
based
antagonists
for
the
treatment
of
malignant
tumors
.
Diseases
Validation
Diseases presenting
"is believed to promote invasion of colon"
symptom
junctional epidermolysis bullosa
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