Frontiers in Oncology,
Journal Year:
2025,
Volume and Issue:
15
Published: March 19, 2025
Lactylation
modifications
have
been
shown
to
be
a
novel
type
of
protein
post-translational
(PTMs),
providing
new
perspective
for
understanding
the
interaction
between
cellular
metabolic
reprogramming
and
epigenetic
regulation.
Studies
that
lactylation
plays
an
important
role
in
occurrence,
development,
angiogenesis,
invasion
metastasis
tumors.
It
can
not
only
regulate
phenotypic
expression
functional
polarization
immune
cells,
but
also
participate
formation
tumor
drug
resistance
through
variety
molecular
mechanisms.
In
this
review,
we
review
latest
research
progress
modification
tumors,
focusing
on
its
mechanism
action
cell
regulation
microenvironment
(TME),
resistance,
aiming
provide
theoretical
basis
ideas
discovery
therapeutic
targets
methods.
Through
in-depth
analysis
modification,
it
is
expected
open
up
direction
treatment
potential
strategies
overcoming
improving
clinical
efficacy.
Brain Research Bulletin,
Journal Year:
2025,
Volume and Issue:
unknown, P. 111292 - 111292
Published: March 1, 2025
Intracerebral
hemorrhage(ICH)
is
a
cerebrovascular
disease
with
high
disability
and
fatality
rate,
inhibition
of
neuronal
cell
death
the
key
to
improve
ICH
injury.
Histone
lactylation
induced
by
lactate,
it
role
in
remains
unclear.
P53
plays
apoptosis.
This
study
aims
investigate
lactate
dehydrogenase
A(LDHA),
factor
production
development
its
regulation
P53.
In
vitro
vivo
model
was
construct
stimulation
hemin
on
PC12
cells
collagenase
IV
injection
C57BL/6J
mice.
Lactate
detected
using
kit.
LDHA
expression
measured
quantitative
real-time
PCR.
Western
blot
performed
detect
protein
level
pan-kla,
apoptosis-related
factors
histone
lactylation.
Impact
evaluated
measuring
viability,
proliferation,
apoptosis,
neurobehavioral
function
assessment
pathological
observation.
Results
showed
that
production,
were
increased
after
ICH.
knockdown
promoted
viability
proliferation
but
suppressed
apoptosis
vitro,
improved
neurological
function,
brain
injury
vivo.
Mechanically,
inhibited
transcription
decreasing
promoter.
Moreover,
overexpression
restored
knockdown.
conclusion,
we
demonstrated
enhanced
promoting
through
increasing
These
results
may
provide
novel
therapeutic
target
for
Cell Death and Disease,
Journal Year:
2025,
Volume and Issue:
16(1)
Published: March 6, 2025
Aberrant
expression
of
programmed
death
ligand-1
(PD-L1)
facilitates
tumor
immune
evasion.
Protein
arginine
methyltransferase
3
(PRMT3),
a
member
type
I
PRMT
family,
mediates
asymmetric
dimethylarginine
(ADMA)
modification
various
substrate
proteins.
This
study
investigates
the
role
PRMT3
in
PD-L1-associated
immunosuppression
hepatocellular
carcinoma
(HCC).
Hepatocyte-specific
knockout
Prmt3
significantly
suppressed
HCC
progression
DEN-CCL4-treated
mice.
Knockout
cells
markedly
increased
CD8+
T
cell
infiltration,
and
reduced
lactate
production
tumors.
interacted
with
pyruvate
dehydrogenase
kinase
1
(PDHK1),
dimethylation
PDHK1
at
363
368
residues
its
activity.
The
R363/368
K
mutant
or
inhibition
by
JX06
blocked
effect
on
production.
treatment
also
attenuated
tumor-promoting
vitro
vivo.
Furthermore,
RNA-seq
analysis
revealed
that
downregulates
tumor-associated
checkpoint,
PD-L1,
tissues.
Chromatin
immunoprecipitation
(ChIP)
assay
demonstrated
promotes
lactate-induced
PD-L1
enhancing
direct
binding
histone
H3
lysine
18
lactylation
(H3K18la)
to
promoter.
Tissue
microarray
showed
positive
correlation
between
patients.
Anti-PD-L1
reversed
PRMT3-induced
growth
restored
infiltration.
Our
research
links
PRMT3-mediated
metabolic
reprogramming
evasion,
revealing
PRMT3-PDHK1-lactate-PD-L1
axis
may
be
potential
target
for
improving
efficacy
immunotherapy
HCC.
Experimental Hematology and Oncology,
Journal Year:
2025,
Volume and Issue:
14(1)
Published: March 8, 2025
Cancer
remains
the
leading
cause
of
mortality
worldwide,
and
emergence
drug
resistance
has
made
identification
new
therapeutic
targets
imperative.
Lactate,
traditionally
viewed
as
a
byproduct
glycolysis
with
limited
ATP-producing
capacity,
recently
gained
recognition
critical
signaling
molecule.
It
plays
key
role
not
only
in
cancer
cell
metabolism
but
also
shaping
tumor
microenvironment
(TME).
Histone
lysine
lactylation,
newly
identified
post-translational
modification,
been
shown
to
influence
range
cellular
processes
cancer.
Current
research
focuses
on
mechanisms
functions
histone
lactylation
cancer,
including
its
gene
expression
regulation,
signal
transduction,
protein
synthesis.
However,
despite
these
advancements,
there
are
still
plenty
barriers
quest
unravel
modification.
The
single-cell
spatial
transcriptomics
may
offer
valuable
insights
for
selecting
targets.
This
review
provides
comprehensive
summary
applications
modification
clinical
settings.
Through
detailed
analysis,
we
identify
challenges
limitations
that
exist
current
landscape.
These
lay
groundwork
future
studies
by
highlighting
promising
directions.
Frontiers in Oncology,
Journal Year:
2025,
Volume and Issue:
15
Published: March 19, 2025
Lactylation
modifications
have
been
shown
to
be
a
novel
type
of
protein
post-translational
(PTMs),
providing
new
perspective
for
understanding
the
interaction
between
cellular
metabolic
reprogramming
and
epigenetic
regulation.
Studies
that
lactylation
plays
an
important
role
in
occurrence,
development,
angiogenesis,
invasion
metastasis
tumors.
It
can
not
only
regulate
phenotypic
expression
functional
polarization
immune
cells,
but
also
participate
formation
tumor
drug
resistance
through
variety
molecular
mechanisms.
In
this
review,
we
review
latest
research
progress
modification
tumors,
focusing
on
its
mechanism
action
cell
regulation
microenvironment
(TME),
resistance,
aiming
provide
theoretical
basis
ideas
discovery
therapeutic
targets
methods.
Through
in-depth
analysis
modification,
it
is
expected
open
up
direction
treatment
potential
strategies
overcoming
improving
clinical
efficacy.
