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Inhibition of mammalian target of rapamycin by rapamycin increases the radiosensitivity of esophageal carcinoma Eca109 cells.
[esophageal carcinoma]
The
aim
of
the
present
study
was
to
investigate
whether
radiation
induces
the
mammalian
target
of
rapamycin
(
Rap
)
(
mTOR
)
signaling
pathway
in
esophageal
carcinoma
Eca
109
cells
,
and
whether
mTOR
inhibition
by
rapamycin
increases
Eca
109
cell
radiosensitivity
.
Changes
in
the
levels
of
mTOR
signaling
pathway
and
DNA
damage-repair
proteins
in
Eca
109
cells
prior
to
and
following
radiation
were
determined
.
The
Eca
109
cells
were
treated
with
Rap
(
0
,
100
,
200
and
400
nmol
/
l
)
in
combination
with
radiation
(
0
,
2
,
4
and
6
Gy
)
.
The
cell
proliferation
inhibition
rate
was
determined
by
MTT
assay
.
The
optimum
Rap
concentration
and
radiation
dose
,
which
appropriately
inhibited
cell
proliferation
,
were
then
selected
for
further
study
.
An
appropriate
combination
of
Rap
and
radiation
for
the
Eca
109
cells
was
also
selected
and
changes
in
the
mTOR
signaling
pathway
,
apoptosis
and
DNA
damage-repair
proteins
,
as
well
as
in
cell
clone
formation
,
survival
curves
,
the
apoptosis
rate
and
radiation-induced
DNA
damage
were
determined
.
The
expression
of
the
mTOR
signaling
pathway
and
DNA
damage-repair
proteins
were
found
to
increase
following
the
irradiation
of
the
Eca
109
cells
.
In
addition
,
Rap
was
found
to
inhibit
the
mTOR
signaling
pathway
and
the
expression
of
the
DNA
damage-repair
proteins
.
At
the
same
radiation
dose
,
with
increasing
Rap
concentration
,
the
proliferation
inhibition
rates
of
the
Eca
109
cells
were
found
to
improve
.
The
clone
formation
and
survival
curves
of
the
experimental
group
were
less
than
those
of
the
control
groups
.
Furthermore
,
the
cell
apoptosis
rate
and
expression
of
cleaved
caspase-
3
and
bax
in
the
experimental
group
were
higher
than
those
of
the
control
groups
,
whereas
the
expression
of
bcl-
2
was
less
than
that
of
the
control
groups
.
The
radiation-induced
DNA
damage
of
the
experimental
group
was
greater
than
that
of
the
control
group
.
The
inhibition
of
mTOR
by
Rap
was
found
to
effectively
inhibit
the
proliferation
,
survival
and
radiation-induced
DNA
damage
repair
of
the
Eca
109
cells
following
irradiation
,
as
well
as
promoting
radiation-induced
apoptosis
,
thereby
increasing
the
radiosensitivity
of
the
esophageal
carcinoma
Eca
109
cells
.
Diseases
Validation
Diseases presenting
"changes in the mtor"
symptom
esophageal carcinoma
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