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Cellular nucleic acid binding protein suppresses tumor cell metastasis and induces tumor cell death by downregulating heterogeneous ribonucleoprotein K in fibrosarcoma cells.
[inclusion body myositis]
Cellular
nucleic
acid
binding
protein
(
CNBP
)
has
been
implicated
in
vertebrate
craniofacial
development
and
in
myotonic
dystrophy
type
2
(
DM
2
)
and
sporadic
inclusion
body
myositis
(
sIBM
)
human
diseases
by
controlling
cell
proliferation
and
survival
to
mediate
neural
crest
expansion
.
CNBP
has
been
found
to
bind
single
-stranded
nucleic
acid
and
promote
rearrangements
of
nucleic
acid
secondary
structure
in
an
ATP-independent
manner
,
acting
as
a
nucleic
acid
chaperone
.
A
variety
of
methods
were
used
,
including
cell
viability
assays
,
wound-scratch
assays
,
chemotaxis
assays
,
invasion
assays
,
circular
dichroic
(
CD
)
spectroscopy
,
NMR
spectroscopy
,
chromatin
immunoprecipitation
,
expression
and
purification
of
recombinant
human
CNBP
,
electrophoretic
mobility
shift
assay
(
EMSA
)
,
surface
plasmon
resonance
(
SPR
)
,
fluorescence
resonance
energy
transfer
(
FRET
)
analyses
,
luciferase
reporter
assay
,
Western
blotting
,
and
isothermal
titration
calorimetry
(
ITC
)
.
Up-regulation
of
CNBP
induced
human
fibrosarcoma
cell
death
and
suppressed
fibrosarcoma
cell
motility
and
invasiveness
.
It
was
found
that
CNBP
transcriptionally
down-regulated
the
expression
of
heterogeneous
ribonucleoprotein
K
(
hnRNP
K
)
through
its
conversion
of
a
G-
rich
sequence
into
G-
quadruplex
in
the
promoter
of
hnRNP
K
.
G-
quadruplex
stabilizing
ligand
tetra-
(
N-
methyl-
4
-
pyridyl
)
porphyrin
(
TMPyP
4
)
could
interact
with
and
stabilize
the
G-
quadruplex
,
resulting
in
downregulation
of
hnRNP
K
transcription
.
CNBP
overexpression
caused
increase
of
cell
death
and
suppression
of
cell
metastasis
through
its
induction
of
G-
quadruplex
formation
in
the
promoter
of
hnRNP
K
resulting
in
hnRNP
K
down-regulation
.
The
present
result
provided
a
new
solution
for
controlling
hnRNP
K
expression
,
which
should
shed
light
on
new
anticancer
drug
design
and
development
.
Diseases
Validation
Diseases presenting
"promote rearrangements of nucleic acid secondary structure in an atp-independent manner"
symptom
inclusion body myositis
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