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Resveratrol prevents rapamycin-induced upregulation of autophagy and selectively induces apoptosis in TSC2-deficient cells.
[lymphangioleiomyomatosis]
The
mammalian
/
mechanistic
target
of
rapamycin
complex
1
(
mTORC
1
)
signaling
pathway
is
hyperactivated
in
a
variety
of
cancers
and
disorders
,
including
lymphangioleiomyomatosis
(
LAM
)
and
tuberous
sclerosis
complex
(
TSC
)
,
which
are
characterized
by
mutations
in
tumor
suppressors
TSC
1
or
TSC
2
.
The
concern
with
the
use
of
mTORC
1
inhibitors
,
such
as
rapamycin
or
its
analogs
(
rapalogs
)
,
is
that
they
cause
upregulation
of
autophagy
and
suppress
the
negative
feedback
loop
to
Akt
,
which
promotes
cell
survival
,
causing
the
therapy
to
be
only
partially
effective
,
and
relapse
occurs
upon
cessation
of
treatment
.
In
this
study
,
we
investigate
the
use
of
rapamycin
in
combination
with
resveratrol
,
a
naturally
occurring
polyphenol
,
in
TSC
2
-
deficient
cells
.
We
tested
whether
such
combination
would
prevent
rapamycin-induced
upregulation
of
autophagy
and
shift
the
cell
fate
toward
apoptosis
.
We
found
that
this
combination
treatment
blocked
rapamycin-induced
upregulation
of
autophagy
and
restored
inhibition
of
Akt
.
Interestingly
,
the
combination
of
rapamycin
and
resveratrol
selectively
promoted
apoptosis
of
TSC
2
-
deficient
cells
.
Thus
,
the
addition
of
resveratrol
to
rapamycin
treatment
may
be
a
promising
option
for
selective
and
targeted
therapy
for
diseases
with
TSC
loss
and
mTORC
1
hyperactivation
.
Diseases
Validation
Diseases presenting
"mtorc1 hyperactivation"
symptom
lymphangioleiomyomatosis
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