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The impact of S6K1 kinase on neuroblastoma cell proliferation is independent of GLI1 signaling.
[esophageal adenocarcinoma]
The
crosstalk
between
Hedgehog
(
HH
)
signaling
and
other
signal
transduction
cascades
has
been
extensively
studied
in
different
cancers
.
In
neuroblastoma
,
mTOR
/
S
6
K
1
signaling
is
known
to
have
a
role
in
the
development
of
this
disease
and
recent
evidence
also
implicates
the
HH
pathway
.
Moreover
,
S
6
K
1
kinase
has
been
shown
to
phosphorylate
GLI
1
,
the
effector
of
HH
signaling
,
promoting
GLI
1
transcriptional
activity
and
oncogenic
function
in
esophageal
adenocarcinoma
.
In
this
study
,
we
examined
the
possible
interplay
of
S
6
K
1
and
GLI
1
signaling
in
neuroblastoma
.
siRNA
knockdowns
were
used
to
suppress
S
6
K
1
and
GLI
1
expression
,
and
the
siRNA
effects
were
validated
by
real-time
PCR
and
Western
blotting
.
Cell
proliferation
analysis
was
performed
with
the
EdU
incorporation
assay
.
Cytotoxic
analysis
with
increasing
concentrations
of
PI
3
K
/
mTOR
and
GLI
inhibitors
,
individually
and
in
combination
,
was
used
to
determine
drug
response
.
Although
knockdown
of
either
S
6
K
1
or
GLI
1
reduces
the
cellular
proliferation
of
neuroblastoma
cells
,
there
is
little
effect
of
S
6
K
1
on
the
expression
of
GLI
1
mRNA
and
protein
and
on
the
capacity
of
GLI
1
to
activate
target
genes
.
No
detectable
phosphorylation
of
GLI
1
is
observed
prior
or
following
S
6
K
1
knockdown
.
GLI
1
overexpression
can
not
rescue
the
reduced
proliferation
elicited
by
S
6
K
1
knockdown
.
Moreover
,
inhibitors
of
PI
3
K
/
mTOR
and
GLI
signaling
reduced
neuroblastoma
cell
growth
,
but
no
additional
growth
inhibitory
effects
were
detected
when
the
two
classes
of
drugs
were
combined
.
Our
results
demonstrate
that
the
impact
of
S
6
K
1
kinase
on
neuroblastoma
cells
is
not
mediated
through
modulation
of
GLI
1
expression
/
activity
.
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esophageal adenocarcinoma
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