Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: Dec. 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.
Molecular Cancer,
Journal Year:
2025,
Volume and Issue:
24(1)
Published: March 5, 2025
Targeting
the
dysregulation
of
epigenetic
mechanisms
in
cancer
has
emerged
as
a
promising
therapeutic
strategy.
Although
significant
rationale
progress
therapies
blocking
cells,
how
regulation
shapes
tumor
microenvironment
(TME)
and
establishes
antitumor
immunity
remains
less
understood.
Recent
study
focus
been
put
on
epigenetic-mediated
changes
fate
immune
including
differentiation,
expansion,
recruitment,
functionalization,
exhaustion
T
natural
killer
(NK)
tumor-associated
macrophages
(TAMs),
dendritic
cells
(DCs),
myeloid-derived
suppressor
(MDSCs),
B
within
TME.
Here,
we
review
latest
molecular
clinical
insights
into
DNA
modifications,
histone
modification,
epitranscriptome-related
regulations
shape
various
cancers.
We
also
discuss
opportunities
for
leveraging
to
improve
immunotherapies.
This
provides
foundations
proposes
future
direction
combination
therapies.
Cell Death and Disease,
Journal Year:
2025,
Volume and Issue:
16(1)
Published: April 15, 2025
Abstract
Functional
CD8
+
T
cell
immunity
is
essential
for
immune
surveillance
and
host
defense
against
infection
tumors.
Epigenetic
mechanisms,
particularly
RNA
modification,
in
controlling
response
not
fully
elucidated.
Here,
by
cell-specific
deletion
of
fat
mass
obesity-associated
protein
(FTO),
a
critical
N6-methyladenosine
(m
6
A)
demethylase,
we
revealed
that
FTO
was
indispensable
adequate
protective
function.
ablation
led
to
considerable
death
activated
cells,
which
attributed
apoptosis.
MeRIP-seq
analysis
an
increase
m
A
methylation
on
Fas
mRNA
FTO-deficient
cells.
The
loss
promoted
expression
via
enhancing
the
stability,
depended
reader
insulin-like
growth
factor-2
mRNA-biding
proteins
3
(IGF2BP3).
Mutation
sites
or
knockdown
IGF2BP3
could
normalize
upregulated
apoptosis
levels
caused
Our
findings
delineate
novel
epigenetic
regulatory
mechanism
FTO-mediated
modification
supporting
survival
effector
responses,
providing
new
insights
into
understanding
post-transcriptional
regulation
immunological
functions
potential
therapeutic
intervention.
Clinical & Experimental Immunology,
Journal Year:
2024,
Volume and Issue:
217(1), P. 57 - 77
Published: March 20, 2024
Abstract
The
enzymatic
core
component
of
m6A
writer
complex,
Mettl3,
plays
a
crucial
role
in
facilitating
the
development
and
progress
gastric
colorectal
cancer
(CRC).
However,
its
underlying
mechanism
regulating
intestinal
inflammation
remains
unclear
poorly
investigated.
First,
characteristics
Mettl3
expression
inflammatory
bowel
diseases
(IBD)
patients
were
examined.
Afterward,
we
generated
mice
line
with
epithelial
cells
(IECs)-specific
deletion
verified
by
various
experiments.
We
continuously
recorded
compared
physiological
status
including
survival
rate
etc.
between
two
groups.
Subsequently,
took
advantage
staining
assays
to
analyze
mucosal
damage
immune
infiltration
Mettl3WT
Mettl3KO
primary
IECs.
Bulk
RNA
sequencing
was
used
pursuit
differential
genes
(DEGs)
associated
signaling
pathways
after
losing
Mettl3.
Pyroptosis-related
proteins
determine
whether
cell
death
caused
pyroptosis.
Eventually,
CyTOF
performed
probe
difference
CD45+
cells,
especially
CD3e+
T-cell
clusters
In
IBD
patients,
highly
expressed
inner-nucleus
IECs
while
significantly
decreased
upon
acute
inflammation.
IECs-specific
KO
triggered
wasting
phenotype
developed
spontaneous
colitis.
rate,
body
weight,
length
observed
from
2
8
weeks
lower
than
mice.
degree
even
more
serious
their
WT
littermate.
demonstrated
that
DEGs
dramatically
enriched
NOD-signaling
due
loss
colonic
epithelium
prone
pyroptosis
revealed
T
have
altered
Mettl3KO.
Furthermore,
there
abnormal
proliferation
CD4+
markedly
exhaustion
CD8
+
severe
is
located
declined
when
occurs.
prevented
developing
Frontiers in Pharmacology,
Journal Year:
2024,
Volume and Issue:
15
Published: July 23, 2024
Asthma
is
a
common
chronic
inflammatory
disease
of
the
lungs
and
airway,
yet
its
subtypes
potential
pathogenesis
have
not
been
completely
elucidated
require
further
study.
With
advances
in
epigenetic
development,
methylation
has
emerged
as
new
direction
for
identifying
decoding
occurrence
subtype
manifestations
asthma.
N
6
-methyladenosine
(m
A),
an
RNA
modification
occurring
-position
adenosine,
prevalent
observed
eukaryotes.
It
exerts
significant
control
over
mRNA
metabolism
by
regulating
alternative
splicing,
stability,
export,
translation.
The
dynamic
process
m
A
plays
crucial
role
asthma
tightly
regulated
three
types
regulators:
writers,
readers,
erasers.
This
article
provides
comprehensive
review
association
between
regulators
asthma,
such
involvement
cells
related
response.
Furthermore,
findings
presented
herein
provide
insights
solid
foundation
research
on
biomarkers
diagnosis
development
personalized
treatment
different
particularly
neutrophilic
eosinophilic
