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Identification of a novel lysyl oxidase-like 2 alternative splicing isoform, LOXL2 Δe13, in esophageal squamous cell carcinoma.
[esophageal squamous cell carcinoma]
Lysyl
oxidase-like
2
(
LOXL
2
)
participates
in
every
stage
of
cancer
progression
and
promotes
invasion
and
metastasis
.
In
this
study
,
we
identified
a
novel
alternative
splicing
isoform
of
LOXL
2
,
namely
LOXL
2
Δe
13
,
which
lacked
exon
13
.
Deletion
of
exon
13
caused
an
open
reading
frame
shift
and
produced
a
truncated
protein
.
LOXL
2
Δe
13
was
expressed
ubiquitously
in
cell
lines
and
tissues
and
was
mainly
localized
to
the
cytoplasm
.
Although
it
showed
impaired
deamination
enzymatic
activity
compared
with
full-length
LOXL
2
,
LOXL
2
Δe
13
promoted
the
cell
mobility
and
invasion
of
esophageal
squamous
cell
carcinoma
(
ESCC
)
cells
to
greater
degrees
.
In
further
research
on
the
mechanisms
,
gene
expression
profiling
and
signaling
pathway
analysis
revealed
that
LOXL
2
Δe
13
induced
the
expression
of
MAPK
8
without
affecting
the
FAK
,
AKT
,
and
ERK
signaling
pathways
.
RNAi-mediated
knockdown
of
MAPK
8
could
block
the
cell
migration
promoted
by
LOXL
2
De
13
,
but
it
had
little
effect
on
that
of
full-length
LOXL
2
.
Our
data
suggest
that
LOXL
2
Δe
13
modulates
the
effects
of
cancer
cell
migration
and
invasion
through
a
different
mechanism
from
that
of
full-length
LOXL
2
and
that
it
may
play
a
very
important
role
in
tumor
carcinogenesis
and
progression
.
