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Glutathione Peroxidase 7 Suppresses Bile Salt-Induced Expression of Pro-Inflammatory Cytokines in Barrett's Carcinogenesis.
[esophageal adenocarcinoma]
Esophageal
adenocarcinoma
(
EAC
)
is
the
most
frequent
malignancy
in
the
esophagus
in
the
US
and
its
incidence
has
been
rising
rapidly
in
the
past
few
decades
.
Chronic
gastroesophageal
reflux
disease
(
GERD
)
,
where
the
esophageal
epithelium
is
abnormally
exposed
to
acid
and
bile
salts
,
is
a
pro-
inflammatory
condition
that
is
the
main
risk
factor
for
the
development
of
Barrett
's
esophagus
(
BE
)
and
its
progression
to
EAC
.
Glutathione
peroxidase
7
(
GPX
7
)
is
frequently
silenced
through
DNA
hypermethylation
during
Barrett
's
tumorigenesis
.
In
this
study
,
we
investigated
the
role
of
GPX
7
in
regulating
the
bile
salts-induced
inflammatory
signaling
in
Barrett
's
carcinogenesis
.
Using
quantitative
real-time
PCR
(
qRT-PCR
)
,
we
demonstrated
a
significant
induction
in
the
expression
levels
of
pro-
inflammatory
cytokines
(
TNF
-α
,
IL
-
1
β
,
IL
-
6
,
and
IL
-
8
)
and
chemokines
(
CXCL-
1
and
CXCL-
2
)
in
esophageal
cells
after
exposure
to
acidic
(
pH
4
)
or
neutral
(
pH
7
)
bile
salts
.
Western
blot
analysis
showed
that
exposure
to
acidic
and
neutral
bile
salts
increased
p
-
NF-
κB-
p
65
(
S
536
)
protein
levels
independent
of
ROS
.
Reconstitution
of
GPX
7
expression
in
EAC
cells
abolished
the
increase
of
p
-
p
65
(
S
536
)
protein
levels
and
mRNA
expression
of
cytokines
and
chemokines
upon
treatment
with
acidic
and
neutral
bile
salts
.
Examination
of
human
primary
EAC
tissues
by
qRT-PCR
demonstrated
significant
overexpression
of
cytokines
(
TNF
-α
,
IL
-
1
β
and
IL
-
8
)
in
EAC
samples
,
as
compared
to
normal
samples
,
with
significant
inverse
correlation
with
GPX
7
expression
level
.
Taken
together
,
the
loss
of
GPX
7
expression
promotes
bile
salt
-induced
activation
of
pro-
inflammatory
cytokines
and
chemokines
;
important
contributors
to
GERD
-associated
Barrett
's
carcinogenesis
.
Diseases
Validation
Diseases presenting
"frequent malignancy"
symptom
esophageal adenocarcinoma
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