Cell Biology and Toxicology,
Journal Year:
2024,
Volume and Issue:
41(1)
Published: Dec. 27, 2024
N-acetyltransferase
10
(NAT10)
is
a
member
of
the
Gcn5-related
(GNAT)
family
and
it
plays
crucial
role
in
various
cellular
processes,
such
as
regulation
cell
mitosis,
post-DNA
damage
response,
autophagy
apoptosis
regulation,
ribosome
biogenesis,
RNA
modification,
other
related
pathways
through
its
intrinsic
protein
acetyltransferase
activities.
Moreover,
NAT10
closely
associated
with
pathogenesis
tumors,
Hutchinson-Gilford
progeria
syndrome
(HGPS),
systemic
lupus
erythematosus,
pulmonary
fibrosis,
depression
host–pathogen
interactions.
In
recent
years,
mRNA
acetylation
has
emerged
prominent
focus
research
due
to
pivotal
regulating
stability
translation.
stands
out
sole
identified
modification
enzyme
responsible
for
acetylation.
There
remains
some
ambiguity
regarding
similarities
differences
NAT10's
actions
on
substrates.
While
involves
both
cases,
which
molecular
mechanism
epigenetic
there
are
significant
disparities
catalytic
mechanisms,
regulatory
pathways,
biological
processes
involved.
Therefore,
this
review
aims
offer
comprehensive
overview
acetyltransferase,
covering
basic
features,
functions,
roles
diseases.
Cell Communication and Signaling,
Journal Year:
2024,
Volume and Issue:
22(1)
Published: Jan. 17, 2024
Abstract
N
4
-acetylcytidine
(ac
C)
is
a
highly
conserved
chemical
modification
widely
found
in
eukaryotic
and
prokaryotic
RNA,
such
as
tRNA,
rRNA,
mRNA.
This
significantly
associated
with
various
human
diseases,
especially
cancer,
its
formation
depends
on
the
catalytic
activity
of
N-acetyltransferase
10
(NAT10),
only
known
protein
that
produces
ac
C.
review
discusses
detection
techniques
regulatory
mechanisms
C
summarizes
correlation
tumor
occurrence,
development,
prognosis,
drug
therapy.
It
also
comments
new
biomarker
for
early
diagnosis
prognosis
prediction
target
MedComm,
Journal Year:
2025,
Volume and Issue:
6(1)
Published: Jan. 1, 2025
Abstract
N4‐acetylcytidine
(ac4C)
modification
is
a
crucial
RNA
widely
present
in
eukaryotic
RNA.
Previous
studies
have
demonstrated
that
ac4C
plays
pivotal
role
viral
infections.
Despite
numerous
highlighting
the
strong
correlation
between
and
cancer
progression,
its
detailed
roles
molecular
mechanisms
normal
physiological
processes
progression
remain
incompletely
understood.
This
review
first
outlines
key
regulatory
enzyme
mediating
modification,
N‐acetyltransferase
10
(NAT10),
including
critical
regulating
stability,
transcriptional
efficiency,
translational
fidelity.
Additionally,
it
systematically
summarizes
essential
functions
of
biological
processes,
stem
cell
fate
determination,
spermatogenesis
oogenesis,
embryonic
development,
cellular
senescence,
bone
remodeling.
Furthermore,
this
delves
into
central
malignant
proliferation,
cycle
arrest,
EMT,
drug
resistance,
death,
metabolism,
tumor
immunotherapy.
It
also
emphasizes
potential
NAT10
as
prognostic
biomarker
therapeutic
target
for
disease
treatment.
In
summary,
clarifies
multifaceted
both
health
explores
NAT10‐targeted
therapies
with
aim
advancing
research
improving
patient
outcomes.
BMC Women s Health,
Journal Year:
2025,
Volume and Issue:
25(1)
Published: Feb. 8, 2025
Ovarian
cancer
(OC)
is
the
most
lethal
gynecological
tumor.
N4-acetylcytidine
(ac4C)
modification,
catalyzed
by
acetyltransferase
NAT10,
involved
in
occurrence
and
development
of
cancers.
This
study
aimed
to
investigate
role
NAT10
OC
underlying
molecular
mechanisms.
The
expression
CAPRIN1
cells
lines
were
measured
using
quantitative
real-time
polymerase
chain
reaction
immunoblotting.
Biological
behaviors
evaluated
EdU,
Transwell,
sphere
formation,
immunoblotting
assays.
mechanism
function
was
analyzed
bioinformatics,
ac4C-
RNA
immunoprecipitation,
actinomycin
D
treatment
assay.
effect
on
progression
vivo
xenograft
tumor
model.
results
indicated
that
highly
expressed
cells.
knockdown
suppressed
cell
proliferation,
migration,
invasiveness,
stemness,
epithelial-mesenchymal
transition
vitro,
impeded
growth
vivo.
Additionally,
found
be
positively
related
OC.
Silencing
inhibited
ac4C
levels
reduced
its
stability.
Moreover,
overexpression
reversed
suppression
invasion,
stemness
caused
knockdown,
while
alone
these
malignant
In
conclusion,
promotes
promoting
cellular
via
upregulating
expression.
Mechanistically,
stabilizes
modification.
These
findings
suggest
may
a
promising
therapy
target
for
