Cancer Medicine,
Journal Year:
2024,
Volume and Issue:
13(11)
Published: June 1, 2024
Lung
cancer
remains
the
foremost
reason
of
cancer-related
mortality,
with
invasion
and
metastasis
profoundly
influencing
patient
prognosis.
N-acetyltransferase
10
(NAT10)
catalyzes
exclusive
N
(4)-acetylcytidine
(ac4C)
modification
in
eukaryotic
RNA.
NAT10
dysregulation
is
linked
to
various
diseases,
yet
its
role
non-small
cell
lung
(NSCLC)
unclear.
Our
study
delves
into
clinical
significance
functional
aspects
NSCLC.
Cell Death and Disease,
Journal Year:
2024,
Volume and Issue:
15(1)
Published: Jan. 5, 2024
Abstract
Chromatin
accessibility
plays
important
roles
in
revealing
the
regulatory
networks
of
gene
expression,
while
its
application
bladder
cancer
is
yet
to
be
fully
elucidated.
Chloride
intracellular
channel
3
(CLIC3)
protein
has
been
reported
associated
with
progression
some
tumors,
whereas
specific
mechanism
CLIC3
tumor
remains
unclear.
Here,
we
screened
for
key
genes
through
identification
transcription
factor
binding
site
clustered
region
(TFCR)
on
basis
chromatin
and
TF
motif.
was
identified
by
joint
profiling
data
TCGA
database.
Clinically,
expression
significantly
elevated
negatively
correlated
patient
survival.
promoted
proliferation
cells
reducing
p21
vitro
vivo.
Mechanistically,
interacted
NAT10
inhibited
function
NAT10,
resulting
downregulation
ac4C
modification
stability
mRNA.
Overall,
these
findings
uncover
an
novel
mRNA
may
act
as
a
potential
therapeutic
target
cancer.
Thoracic Cancer,
Journal Year:
2024,
Volume and Issue:
15(10), P. 820 - 829
Published: Feb. 26, 2024
N-acetyltransferase
10
(NAT10)
serves
as
a
critical
enzyme
in
mediating
the
N4-acetylcytidine
(ac4C)
that
ensures
RNA
stability
and
effective
translation
processes.
The
role
of
NAT10
driving
advancement
breast
cancer
remains
uninvestigated.
Nature Communications,
Journal Year:
2024,
Volume and Issue:
15(1)
Published: March 8, 2024
Abstract
Translational
control
is
crucial
for
protein
production
in
various
biological
contexts.
Here,
we
use
Ribo-seq
and
RNA-seq
to
show
that
genes
related
oxidative
phosphorylation
are
translationally
downregulated
during
heart
regeneration.
We
find
Nat10
regulates
the
expression
of
Uqcr11
Uqcrb
mRNAs
mouse
human
cardiomyocytes.
In
mice,
overexpression
cardiomyocytes
promotes
cardiac
regeneration
improves
function
after
injury.
Conversely,
treating
neonatal
mice
with
Remodelin—a
pharmacological
inhibitor—or
genetically
removing
from
their
both
inhibit
Mechanistically,
suppresses
independently
its
ac4C
enzyme
activity.
This
suppression
weakens
mitochondrial
respiration
enhances
glycolytic
capacity
cardiomyocytes,
leading
metabolic
reprogramming.
also
observe
P7
male
pig
hearts
compared
P1
controls.
The
levels
lower
female
failing
than
non-failing
hearts.
further
identify
specific
binding
regions
Nat10,
validate
pro-proliferative
effects
derived
embryonic
stem
cells.
Our
findings
indicate
an
epigenetic
regulator
could
potentially
become
a
clinical
target.
Cellular and Molecular Life Sciences,
Journal Year:
2024,
Volume and Issue:
81(1)
Published: Feb. 3, 2024
Abstract
N4
acetylcytidine
(ac4C)
modification
mainly
occurs
on
tRNA,
rRNA,
and
mRNA,
playing
an
important
role
in
the
expression
of
genetic
information.
However,
it
is
still
unclear
whether
microRNAs
have
undergone
ac4C
their
potential
physiological
pathological
functions.
In
this
study,
we
identified
that
NAT10/THUMPD1
acetylates
primary
(pri-miRNAs)
with
modification.
Knockdown
NAT10
suppresses
augments
levels
mature
miRNAs
pri-miRNAs,
respectively.
Molecular
mechanism
studies
found
pri-miRNA
promotes
processing
into
precursor
miRNA
(pre-miRNA)
by
enhancing
interaction
DGCR8,
thereby
increasing
biogenesis
miRNA.
attenuates
oncogenic
characters
lung
cancer
cells
regulating
production
cancers.
Moreover,
highly
expressed
various
clinical
cancers
negatively
correlated
poor
prognosis.
Thus,
our
results
reveal
plays
a
crucial
initiation
progression
modulating
to
affect
production,
which
would
provide
attractive
therapeutic
strategy
for
Cancer Medicine,
Journal Year:
2024,
Volume and Issue:
13(11)
Published: June 1, 2024
Lung
cancer
remains
the
foremost
reason
of
cancer-related
mortality,
with
invasion
and
metastasis
profoundly
influencing
patient
prognosis.
N-acetyltransferase
10
(NAT10)
catalyzes
exclusive
N
(4)-acetylcytidine
(ac4C)
modification
in
eukaryotic
RNA.
NAT10
dysregulation
is
linked
to
various
diseases,
yet
its
role
non-small
cell
lung
(NSCLC)
unclear.
Our
study
delves
into
clinical
significance
functional
aspects
NSCLC.
