Frontiers in Immunology,
Год журнала:
2024,
Номер
15
Опубликована: Дек. 2, 2024
N1-methyladenosine
(m1A)
modification
is
an
epigenetic
change
that
occurs
on
RNA
molecules,
regulated
by
a
suite
of
enzymes
including
methyltransferases
(writers),
demethylases
(erasers),
and
m1A-recognizing
proteins
(readers).
This
significantly
impacts
the
function
various
biological
processes
affecting
structure,
stability,
translation,
metabolism,
gene
expression
RNA.
Thereby,
m1A
closely
associated
with
occurrence
progression
cancer.
review
aims
to
explore
role
in
tumor
immunity.
affects
immune
responses
directly
regulating
cells
indirectly
modulating
microenvironment.
Besides,
we
also
discuss
implications
m1A-mediated
metabolic
reprogramming
its
nexus
checkpoint
inhibitors,
unveiling
promising
avenues
for
immunotherapeutic
intervention.
Additionally,
m1AScore,
established
based
patterns
modification,
can
be
used
predict
prognosis
guide
personalized
therapy.
Our
underscores
significance
as
burgeoning
frontier
cancer
biology
immuno-oncology,
potential
revolutionize
treatment
strategies.
Drug
resistance
in
cancer
cells
significantly
diminishes
treatment
efficacy,
leading
to
recurrence
and
metastasis.
A
critical
factor
contributing
this
is
the
epigenetic
alteration
of
gene
expression
via
RNA
modifications,
such
as
N6-methyladenosine
(m6A),
N1-methyladenosine
(m1A),
5-methylcytosine
(m5C),
7-methylguanosine
(m7G),
pseudouridine
(Ψ),
adenosine-to-inosine
(A-to-I)
editing.
These
modifications
are
pivotal
regulating
splicing,
translation,
transport,
degradation,
stability.
Governed
by
"writers,"
"readers,"
"erasers,"
impact
numerous
biological
processes
progression,
including
cell
proliferation,
stemness,
autophagy,
invasion,
apoptosis.
Aberrant
can
lead
drug
adverse
outcomes
various
cancers.
Thus,
targeting
modification
regulators
offers
a
promising
strategy
for
overcoming
enhancing
efficacy.
This
review
consolidates
recent
research
on
role
prevalent
resistance,
with
focus
m6A,
m1A,
m5C,
m7G,
Ψ,
A-to-I
Additionally,
it
examines
regulatory
mechanisms
linked
underscores
existing
limitations
field.
Abstract
RNA
modifications
are
emerging
as
critical
cancer
regulators
that
influence
tumorigenesis
and
progression.
Key
modifications,
such
N6‐methyladenosine
(m
6
A)
5‐methylcytosine
5
C),
implicated
in
various
cellular
processes.
These
regulated
by
proteins
write,
erase,
read
modulate
stability,
splicing,
translation,
degradation.
Recent
studies
have
highlighted
their
roles
metabolic
reprogramming,
signaling
pathways,
cell
cycle
control,
which
essential
for
tumor
proliferation
survival.
Despite
these
scientific
advances,
the
precise
mechanisms
affect
remain
inadequately
understood.
This
review
comprehensively
examines
role
play
proliferation,
metastasis,
programmed
death,
including
apoptosis,
autophagy,
ferroptosis.
It
explores
effects
on
epithelial–mesenchymal
transition
(EMT)
immune
microenvironment,
particularly
metastasis.
Furthermore,
modifications’
potential
therapies,
conventional
treatments,
immunotherapy,
targeted
is
discussed.
By
addressing
aspects,
this
aims
to
bridge
current
research
gaps
underscore
therapeutic
of
targeting
improve
treatment
strategies
patient
outcomes.
Advanced Science,
Год журнала:
2025,
Номер
unknown
Опубликована: Фев. 28, 2025
Abstract
Epigenetic
modifications
serve
as
crucial
molecular
switches
for
pathological
fibrosis;
howbeit
the
role
of
m
1
A
in
this
condition
remains
enigmatic.
Herein,
it
is
found
that
ALKBH3
exerts
a
pro‐fibrotic
effect
skin
fibrosis
by
reshaping
N6‐methyladenosine
(m
6
A)
RNA
modification
pattern.
First,
exhibited
specific
upregulation
within
hypertrophic
scars
(HTS),
accompanied
N1‐methyladenosine
hypomethylation.
Moreover,
multiomics
analyses
identified
METTL3,
critical
writer
enzyme
involved
modification,
downstream
candidate
target
ALKBH3.
Therapeutically,
ablation
inhibited
progression
HTS
both
vitro
and
vivo,
while
exogenous
replenishment
METTL3
counteracted
antifibrotic
effect.
Mechanistically,
recognizes
methylation
sites
prevents
YTHDF2‐dependent
mRNA
decay
transcript.
Subsequently,
stabilizes
collagen
type
I
alpha
chain
(
COL1A1
)
fibronectin1
FN1
mRNAs,
two
major
components
extracellular
matrix,
therefore
eliciting
transformation
HTS.
This
observation
bridges
understanding
link
between
methylation,
fundamental
modifications,
underscoring
participation
“RNA
crosstalk”
events.
Current Issues in Molecular Biology,
Год журнала:
2025,
Номер
47(4), С. 266 - 266
Опубликована: Апрель 9, 2025
Current
research
discusses
the
putative
importance
of
RNA
modification
in
tumor
diseases.
These
modifications
include
predominantly
pseudouridinylation,
ortho-methylations
on
ribose
residues,
as
well
methylations
organic
bases.
Such
chemical
directly
influence
fundamental
properties
such
transcript
stability,
alternative
splicing,
and
translation
efficiency,
all
which
are
basic
requirements
for
(tumor)
cell
proliferation,
metabolism,
migration,
apoptosis
resistance,
etc.
In
this
comparative
study,
two
RNA-modifying
factors,
pseudouridine
synthase
7
(PUS7,
pseudouridinylation)
WT1-associated
protein
(WTAP,
m6A
methylation),
were
identified
using
data
from
human
renal
carcinoma
(RCC)
tumors.
PUS7
WTAP
showed
a
statistically
significant
correlation
with
relevant
proliferation
prognosis
markers
CXCR4,
TP53,
PTEN,
NRAS,
immune
checkpoints
HLA-G
LGALS9
associated
effect
overall
survival.
Furthermore,
analyses
also
further
target
mRNAs
biology
WTAP.
particular,
components
direct
relevance
mitosis,
cycle,
division,
WNT
pathway,
identified.
Nucleic
acids
are
genetic
information-carrying
molecules
inside
cells.
Apart
from
basic
nucleotide
building
blocks,
there
exist
various
naturally
occurring
chemical
modifications
on
nucleobase
and
ribose
moieties,
which
greatly
increase
the
encoding
complexity
of
nuclei
acids,
contribute
to
alteration
nucleic
acid
structures,
play
versatile
regulation
roles
in
gene
expression.
To
study
functions
certain
biological
contexts,
robust
tools
specifically
label
identify
these
macromolecules
their
modifications,
illuminate
structures
highly
necessary.
In
this
review,
we
summarize
recent
technique
advances
using
enzyme-mediated
reactions
structures.
By
highlighting
principles
techniques,
aim
present
a
perspective
advancement
field
as
well
offer
insights
into
developing
specific
precise
enzyme
catalysis
utilized
for
modifications.
BMC Cardiovascular Disorders,
Год журнала:
2024,
Номер
24(1)
Опубликована: Авг. 16, 2024
Heart
failure
(HF),
which
is
caused
by
cardiac
overload
and
injury,
linked
to
significant
mortality.
Writers
of
RNA
modification
(WRMs)
play
a
crucial
role
in
the
regulation
epigenetic
processes
involved
immune
response
cardiovascular
disease.
However,
potential
roles
these
writers
immunological
milieu
HF
remain
unknown.
We
comprehensively
characterized
expressions
28
WRMs
using
datasets
GSE145154
GSE141910
map
microenvironment
patients.
Based
on
expression
WRMs,
cells
were
scored.
Single-cell
transcriptomics
analysis
(GSE145154)
revealed
dysregulation
as
well
differential
from
non-HF
(NHF)
samples.
WRM-scored
positively
correlated
with
response,
high
WRM
score
group
exhibited
elevated
cell
infiltration.
are
differentiation
T
myeloid
cells.
scores
subtypes
significantly
reduced
compared
NHF
group.
identified
myogenesis-related
resident
macrophage
population
heart,
Macro-MYL2,
that
was
an
increased
cardiomyocyte
structural
genes
(MYL2,
TNNI3,
TNNC1,
TCAP,
TNNT2)
regulated
TRMT10C.
pattern,
data
(GSE141910)
two
distinct
clusters
samples,
each
functional
enrichments
characteristics.
Our
study
demonstrated
relationship
between
HF,
novel
population,
myogenesis.
These
results
provide
perspective
underlying
mechanisms
therapeutic
targets
for
HF.
Further
experiments
required
validate
Macro-MYL2
subtype
milieu.
Biomolecules and Biomedicine,
Год журнала:
2024,
Номер
24(6), С. 1827 - 1847
Опубликована: Июль 3, 2024
Recent
discoveries
in
mRNA
modification
have
highlighted
N1-methyladenosine
(m1A),
but
its
role
preeclampsia
(PE)
pathogenesis
remains
unclear.
In
this
study,
we
utilized
methylated
RNA
immunoprecipitation
sequencing
(MeRIP-seq)
and
(RNA-seq)
to
identify
m1A
peaks
the
expression
profile
of
decidua
humans
with
early-onset
PE
(EPE),
late-onset
(LPE),
normal
pregnancy
(NP).
We
assessed
patterns
preeclamptic
using
10
modulators.
Our
bioinformatic
analysis
focused
on
differentially
mRNAs
(DMGs)
expressed
(DEGs)
pairwise
comparisons
EPE
vs.
NP,
LPE
LPE,
as
well
m1A-related
DEGs.
The
identified
3110,
2801,
2818
DMGs,
respectively.
discerned
three
different
from
data.
Further
revealed
that
key
PE-related
DMGs
DEGs
predominantly
influence
signaling
pathways
critical
for
decidualization,
including
cAMP,
MAPK,
PI3K-Akt,
Notch,
TGF-β
pathways.
Additionally,
these
modifications
impact
related
vascular
smooth
muscle
contraction,
estrogen
signaling,
relaxin
contributing
dysfunction.
findings
demonstrate
exhibits
unique
gene
profiles
significantly
alter
essential
both
decidualization
These
differences
provide
valuable
insights
into
molecular
mechanisms
influencing
process
function
PE.
regulators
could
potentially
serve
potent
biomarkers
or
therapeutic
targets
PE,
warranting
further
investigation.