Cell Communication and Signaling,
Journal Year:
2024,
Volume and Issue:
22(1)
Published: Jan. 30, 2024
Abstract
N1-methyladenosine
(m1A)
is
a
post-transcriptionally
modified
RNA
molecule
that
plays
pivotal
role
in
the
regulation
of
various
biological
functions
and
activities.
Especially
cancer
cell
invasion,
proliferation
cycle
regulation.
Over
recent
years,
there
has
been
burgeoning
interest
investigating
m1A
modification
RNA.
Most
studies
have
focused
on
enrichment
areas
different
regions.
This
review
provides
comprehensive
overview
methodologies
employed
for
detection
modification.
Furthermore,
this
delves
into
key
players
modification,
known
as
“writers,”
“erasers,”
“readers.”
by
methyltransferases,
or
writers,
such
TRMT6,
TRMT61A,
TRMT61B,
TRMT10C,
NML,
and,
removed
demethylases,
erasers,
including
FTO
ALKBH1,
ALKBH3.
It
recognized
m1A-binding
proteins
YTHDF1,
TYHDF2,
TYHDF3,
TYHDC1,
also
“readers”.
Additionally,
we
explore
intricate
relationship
between
its
regulators
their
implications
development
progression
specific
types
cancer,
discuss
how
can
potentially
facilitate
discovery
novel
approaches
diagnosis,
treatment,
prognosis.
Our
summary
methylated
adenosine
methods
regulatory
mechanisms
cancers
useful
insights
Signal Transduction and Targeted Therapy,
Journal Year:
2022,
Volume and Issue:
7(1)
Published: Sept. 22, 2022
RNA
modifications
have
become
hot
topics
recently.
By
influencing
processes,
including
generation,
transportation,
function,
and
metabolization,
they
act
as
critical
regulators
of
cell
biology.
The
immune
abnormality
in
human
diseases
is
also
a
research
focus
progressing
rapidly
these
years.
Studies
demonstrated
that
participate
the
multiple
biological
processes
cells,
development,
differentiation,
activation,
migration,
polarization,
thereby
modulating
responses
are
involved
some
related
diseases.
In
this
review,
we
present
existing
knowledge
functions
underlying
mechanisms
modifications,
N6-methyladenosine
(m6A),
5-methylcytosine
(m5C),
N1-methyladenosine
(m1A),
N7-methylguanosine
(m7G),
N4-acetylcytosine
(ac4C),
pseudouridine
(Ψ),
uridylation,
adenosine-to-inosine
(A-to-I)
editing,
summarize
their
roles
Via
regulating
can
pathogenesis
diseases,
such
cancers,
infection,
inflammatory
autoimmune
We
further
highlight
challenges
future
directions
based
on
knowledge.
All
all,
review
will
provide
helpful
well
novel
ideas
for
researchers
area.
Molecular Cancer,
Journal Year:
2023,
Volume and Issue:
22(1)
Published: June 30, 2023
Divergent
N6-methyladenosine
(m6A)
modifications
are
dynamic
and
reversible
posttranscriptional
RNA
that
mediated
by
m6A
regulators
or
methylation
regulators,
i.e.,
methyltransferases
("writers"),
demethylases
("erasers"),
m6A-binding
proteins
("readers").
Aberrant
associated
with
cancer
occurrence,
development,
progression,
prognosis.
Numerous
studies
have
established
aberrant
function
as
either
tumor
suppressors
oncogenes
in
multiple
types.
However,
the
functions
mechanisms
of
remain
largely
elusive
should
be
explored.
Emerging
suggest
can
modulated
epigenetic
modifications,
namely,
ubiquitination,
SUMOylation,
acetylation,
methylation,
phosphorylation,
O-GlcNAcylation,
ISGylation,
lactylation
via
noncoding
action,
cancer.
This
review
summarizes
current
roles
The
for
modification
genesis
segregated.
will
improve
understanding
regulatory
regulators.
Molecular Cancer,
Journal Year:
2022,
Volume and Issue:
21(1)
Published: July 18, 2022
Abstract
The
resistance
of
tumor
cells
to
therapy
severely
impairs
the
efficacy
treatment,
leading
recurrence
and
metastasis
various
cancers.
Clarifying
underlying
mechanisms
therapeutic
may
provide
new
strategies
for
overcoming
cancer
resistance.
N6-methyladenosine
(m6A)
is
most
prevalent
RNA
modification
in
eukaryotes,
involved
regulation
splicing,
translation,
transport,
degradation,
stability
processing,
thus
affecting
several
physiological
processes
progression.
As
a
novel
type
multifunctional
non-coding
RNAs
(ncRNAs),
circular
(circRNAs)
have
been
demonstrated
play
vital
roles
anticancer
therapy.
Currently,
accumulating
studies
revealed
mutual
m6A
circRNAs,
their
interaction
can
further
influence
sensitivity
treatment.
In
this
review,
we
mainly
summarized
recent
advances
circRNAs
modulation
resistance,
as
well
interplay
potential
mechanisms,
providing
promising
insights
future
directions
reversal
cancer.
Drug Resistance Updates,
Journal Year:
2024,
Volume and Issue:
73, P. 101063 - 101063
Published: Feb. 1, 2024
This
study
aims
to
explore
the
function
and
mechanism
of
G
Protein-coupled
receptor
class
C
group
5
member
A
(GPRC5A)
in
docetaxel-resistance
liver
metastasis
breast
cancer.
Molecular Cancer,
Journal Year:
2023,
Volume and Issue:
22(1)
Published: March 1, 2023
Abstract
N6-methyladenosine
(m
6
A)
methylation
is
the
most
universal
internal
modification
in
eukaryotic
mRNA.
With
elaborate
functions
executed
by
m
A
writers,
erasers,
and
readers,
modulation
involved
myriad
physiological
pathological
processes.
Extensive
studies
have
demonstrated
diverse
tumours,
with
effects
on
tumorigenesis,
metastasis,
resistance.
Recent
evidence
has
revealed
an
emerging
role
of
tumour
immunoregulation,
divergent
patterns
been
microenvironment.
To
depict
regulatory
immune
microenvironment
(TIME)
its
effect
evasion,
this
review
focuses
TIME,
which
characterized
hypoxia,
metabolic
reprogramming,
acidity,
immunosuppression,
outlines
A-regulated
TIME
evasion
under
stimuli.
Furthermore,
anti-tumour
cells
are
summarized.
Clinical and Translational Medicine,
Journal Year:
2023,
Volume and Issue:
13(10)
Published: Oct. 1, 2023
Background
N6-methyladenosine
(m6A),
the
most
prevalent
internal
mRNA
modification
in
eukaryotes,
is
added
by
m6A
methyltransferases,
removed
demethylases
and
recognised
m6A-binding
proteins.
This
significantly
influences
carious
facets
of
RNA
metabolism
plays
a
pivotal
role
cellular
physiological
processes.
Main
body
Pre-mRNA
alternative
splicing,
process
that
generates
multiple
splice
isoforms
from
multi-exon
genes,
contributes
to
protein
diversity
mammals.
Moreover,
presence
crosstalk
between
with
modifications
on
pre-mRNAs
exerting
regulatory
control,
has
been
established.
The
modulates
splicing
patterns
recruiting
specific
RNA-binding
proteins
(RBPs)
regulate
or
directly
influencing
interaction
RBPs
their
target
RNAs.
Conversely,
can
impact
deposition
recognition
mRNAs.
integration
expanded
scope
therapeutic
strategies
for
cancer
treatment,
while
offers
novel
insights
into
mechanistic
methylation
initiation
progression.
Conclusion
review
aims
highlight
biological
functions
machinery
its
implications
tumourigenesis.
Furthermore,
we
discuss
clinical
relevance
understanding
m6A-dependent
tumour
therapies.
Advanced Science,
Journal Year:
2024,
Volume and Issue:
11(13)
Published: Jan. 21, 2024
Abstract
N6‐methyladenosine
(m
6
A)
modification
orchestrates
cancer
formation
and
progression
by
affecting
the
tumor
microenvironment
(TME).
For
hepatocellular
carcinoma
(HCC),
immune
evasion
angiogenesis
are
characteristic
features
of
its
TME.
The
role
YTH
RNA
binding
protein
2
(YTHDF2),
as
an
m
A
reader,
in
regulating
HCC
TME
not
fully
understood.
Herein,
it
is
discovered
that
trimethylated
histone
H3
lysine
4
27
acetylation
promoter
region
YTHDF2
enhanced
expression
HCC,
upregulated
predicted
a
worse
prognosis.
Animal
experiments
demonstrated
Ythdf2
depletion
inhibited
spontaneous
formation,
while
overexpression
promoted
xenografted
progression.
Mechanistically,
recognized
5′‐untranslational
ETS
variant
transcription
factor
5
(ETV5)
mRNA
recruited
eukaryotic
translation
initiation
3
subunit
B
to
facilitate
translation.
Elevated
ETV5
induced
programmed
death
ligand‐1
vascular
endothelial
growth
A,
thereby
promoting
angiogenesis.
Targeting
via
small
interference
RNA‐containing
aptamer/liposomes
successfully
both
Together,
this
findings
reveal
potential
application
prognosis
targeted
treatment.
Signal Transduction and Targeted Therapy,
Journal Year:
2024,
Volume and Issue:
9(1)
Published: May 22, 2024
Abstract
Immunotherapy
represented
by
anti-PD-(L)1
and
anti-CTLA-4
inhibitors
has
revolutionized
cancer
treatment,
but
challenges
related
to
resistance
toxicity
still
remain.
Due
the
advancement
of
immuno-oncology,
an
increasing
number
novel
immunoregulatory
targets
mechanisms
are
being
revealed,
with
relevant
therapies
promising
improve
clinical
immunotherapy
in
foreseeable
future.
Therefore,
comprehending
larger
picture
is
important.
In
this
review,
we
analyze
summarize
current
landscape
preclinical
translational
mechanistic
research,
drug
development,
trials
that
brought
about
next-generation
pharmacological
anti-cancer
agents
candidates
beyond
classical
immune
checkpoint
inhibitors.
Along
further
clarification
immunobiology
advances
antibody
engineering,
targeting
additional
inhibitory
checkpoints,
including
LAG-3,
TIM-3,
TIGIT,
CD47,
B7
family
members
becoming
important
part
research
discovery,
as
structurally
functionally
optimized
agonists
co-stimulatory
molecules
T
cells.
Exemplified
bispecific
cell
engagers,
newly
emerging
bi-specific
multi-specific
antibodies
can
provide
considerable
benefits.
Next-generation
also
include
epigenetic
drugs
cytokine-based
therapeutics.
Cell
therapies,
vaccines,
oncolytic
viruses
not
covered
review.
This
comprehensive
review
might
aid
development
fastest
possible
adoption
effective
immuno-oncology
modalities
for
benefit
patients.