Cancers,
Journal Year:
2025,
Volume and Issue:
17(5), P. 788 - 788
Published: Feb. 25, 2025
Ovarian
cancer
is
the
fifth
leading
cause
of
cancer-related
death
among
women,
which
one
most
common
gynecological
cancers
worldwide.
Although
several
cytoreductive
surgeries
and
chemotherapies
have
been
attempted
to
address
ovarian
cancer,
disease
still
shows
poor
prognosis
survival
rates
due
prevalent
metastasis.
Peritoneal
metastasis
recognized
as
primary
route
metastatic
progression
in
cancer.
It
causes
severe
symptoms
patients,
but
it
generally
difficult
detect
at
an
early
stage.
Current
anti-cancer
therapy
insufficient
completely
treat
its
high
recurrence
resistance.
Therefore,
developing
strategies
for
treating
requires
a
deeper
understanding
tumor
microenvironment
(TME)
identification
effective
therapeutic
targets
through
precision
oncology.
Given
that
various
signaling
pathways,
including
TGF-β,
NF-κB,
PI3K/AKT/mTOR
influence
progression,
their
activity
significance
can
vary
depending
on
type.
In
these
pathways
are
particularly
important,
they
not
only
drive
also
impact
TME,
contributes
potential.
The
TME
plays
critical
role
driving
features
altered
immunologic
interactions.
Recent
advances
focused
targeting
distinct
improve
treatment
outcomes.
Deciphering
complex
interaction
between
immune
populations
contributing
provides
opportunity
enhance
efficacy.
Hereby,
this
review
highlights
mechanisms
immunological
interactions
understand
improved
immunotherapy
against
Cells,
Journal Year:
2025,
Volume and Issue:
14(7), P. 511 - 511
Published: March 29, 2025
Oxidative
stress
(OS)
is
an
established
hallmark
of
cancer
and
neurodegenerative
disorders
(NDDs),
which
contributes
to
genomic
instability
neuronal
loss.
This
review
explores
the
contrasting
role
OS
in
stem
cells
(CSCs)
NDDs.
Elevated
levels
reactive
oxygen
species
(ROS)
contribute
promote
tumor
initiation
progression
CSCs,
while
NDDs
such
as
Alzheimer’s
Parkinson’s
disease,
accelerates
death
impairs
cellular
repair
mechanisms.
Both
scenarios
involve
disruption
delicate
balance
between
pro-oxidant
antioxidant
systems,
leads
chronic
oxidative
stress.
Notably,
CSCs
neurons
display
alterations
redox-sensitive
signaling
pathways,
including
Nrf2
NF-κB,
influence
cell
survival,
proliferation,
differentiation.
Mitochondrial
dynamics
further
illustrate
these
differences:
enhanced
function
supports
adaptability
whereas
impairments
heighten
vulnerability.
Understanding
common
mechanisms
OS-induced
redox
imbalance
may
provide
insights
for
developing
interventions,
addressing
aging
hallmarks,
potentially
mitigating
or
preventing
both
Proceedings of the National Academy of Sciences,
Journal Year:
2025,
Volume and Issue:
122(2)
Published: Jan. 8, 2025
Understanding
the
role
of
metabolic
processes
during
inner
ear
development
is
essential
for
identifying
targets
hair
cell
(HC)
regeneration,
as
choices
play
a
crucial
in
proliferation
and
differentiation.
Among
processes,
growing
evidence
shows
that
glucose
metabolism
closely
related
to
organ
development.
However,
mammalian
HC
regeneration
remains
unclear.
In
this
study,
we
found
glycolytic
highly
active
mouse
human
cochlear
prosensory
epithelium
expansion.
Using
organoids,
revealed
activity
nonsensory
epithelial
cells
was
predominantly
dominated
by
pyruvate
kinase
M2
(PKM2).
Deletion
PKM2
induced
switch
from
glycolysis
oxidative
phosphorylation,
impairing
organoid
formation.
Furthermore,
conditional
loss
progenitors
hindered
sensory
morphogenesis,
demonstrated
knockout
mice.
Mechanistically,
generated
catalysis
then
converted
into
lactate,
which
lactylates
histone
H3,
regulating
transcription
key
genes
Specifically,
accumulated
lactate
causes
H3
lactylation
at
lysine
9
(H3K9la),
upregulating
expression
Sox
family
factors
through
epigenetic
modification.
Moreover,
overexpression
supporting
(SCs)
triggered
reprogramming
enhanced
generation
cultured
explants.
Our
findings
uncover
molecular
mechanism
formation
driven
glycolysis-lactate
flow
suggest
unique
approaches
regeneration.
Military Medical Research,
Journal Year:
2025,
Volume and Issue:
12(1)
Published: Feb. 11, 2025
Abstract
Cancer
recurrence,
driven
by
the
phenomenon
of
tumor
dormancy,
presents
a
formidable
challenge
in
oncology.
Dormant
cancer
cells
have
ability
to
evade
detection
and
treatment,
leading
relapse.
This
review
emphasizes
urgent
need
comprehend
dormancy
its
implications
for
recurrence.
Despite
notable
advancements,
significant
gaps
remain
our
understanding
mechanisms
underlying
lack
reliable
biomarkers
predicting
provides
comprehensive
analysis
cellular,
angiogenic,
immunological
aspects
dormancy.
It
highlights
current
therapeutic
strategies
targeting
dormant
cells,
particularly
combination
therapies
immunotherapies,
which
hold
promise
preventing
By
elucidating
these
proposing
innovative
research
methodologies,
this
aims
deepen
ultimately
facilitating
development
more
effective
recurrence
improving
patient
outcomes.
Cells,
Journal Year:
2024,
Volume and Issue:
13(22), P. 1924 - 1924
Published: Nov. 20, 2024
Identifying
definitive
biomarkers
that
predict
clinical
response
and
resistance
to
immunotherapy
remains
a
critical
challenge.
One
emerging
factor
is
extracellular
acidosis
in
the
tumor
microenvironment
(TME),
which
significantly
impairs
immune
cell
function
contributes
failure.
However,
acidic
conditions
TME
disrupt
interaction
between
cancer
cells,
driving
tumor-infiltrating
T
cells
NK
into
an
inactivated,
anergic
state.
Simultaneously,
promotes
recruitment
activation
of
immunosuppressive
such
as
myeloid-derived
suppressor
regulatory
(Tregs).
Notably,
acidity
enhances
exosome
release
from
Tregs,
further
amplifying
immunosuppression.
Tumor
thus
acts
"protective
shield,"
neutralizing
anti-tumor
responses
transforming
pro-tumor
allies.
Therefore,
targeting
lactate
metabolism
has
emerged
promising
strategy
overcome
this
barrier,
with
approaches
including
buffer
agents
neutralize
pH
inhibitors
block
production
or
transport,
thereby
restoring
efficacy
TME.
Recent
discoveries
have
identified
genes
involved
(pHe)
regulation,
presenting
new
therapeutic
targets.
Moreover,
ongoing
research
aims
elucidate
molecular
mechanisms
acidification
develop
treatments
modulate
levels
enhance
outcomes.
Additionally,
future
studies
are
crucial
validate
safety
pHe-targeted
therapies
patients.
Thus,
review
explores
regulation
pHe
its
potential
role
improving
immunotherapy.
Journal of Translational Medicine,
Journal Year:
2025,
Volume and Issue:
23(1)
Published: Feb. 14, 2025
Abstract
Lung
cancer
remains
the
leading
cause
of
cancer-related
mortality
globally,
necessitating
continual
exploration
novel
therapeutic
targets.
The
phosphoinositide
3-kinase
(PI3K)
signaling
pathway
plays
a
pivotal
role
in
oncogenic
processes,
including
cell
growth,
survival,
metabolism
and
immune
modulation.
This
comprehensive
review
delineates
distinct
roles
PI3K
subtypes—PI3Kα,
PI3Kβ,
PI3Kγ
PI3Kδ—in
lung
pathogenesis
progression.
We
evaluate
current
landscape
inhibitors,
transitioning
from
non-selective
early-generation
compounds
to
isoform-specific
agents,
highlighting
their
clinical
efficacy,
resistance
mechanisms
potential
combination
strategies.
Furthermore,
intricate
interplay
between
tumor
microenvironment
is
explored,
elucidating
how
modulation
can
enhance
immunotherapeutic
responses.
Metabolic
reprogramming
driven
by
also
dissected,
revealing
vulnerabilities
that
be
therapeutically
exploited.
Despite
promising
advancements,
challenges
such
as
adverse
effects
underscore
need
for
personalized
medicine
approaches
development
next-generation
inhibitors.
underscores
multifaceted
advocates
integrated
strategies
harness
its
full
potential,
paving
way
improved
patient
outcomes.
Antioxidants,
Journal Year:
2025,
Volume and Issue:
14(1), P. 115 - 115
Published: Jan. 20, 2025
The
role
of
mitochondria
as
the
electric
engine
cells
is
well
established.
Over
past
two
decades,
accumulating
evidence
has
pointed
out
that,
despite
presence
a
highly
active
glycolytic
pathway
(Warburg
effect),
functional
and
even
upregulated
mitochondrial
respiration
occurs
in
cancer
to
meet
need
high
energy
biosynthetic
demand
sustain
their
anabolic
growth.
Mitochondria
are
also
primary
source
intracellular
ROS.
Cancer
maintain
moderate
levels
ROS
promote
tumorigenesis,
metastasis,
drug
resistance;
indeed,
once
cytotoxicity
threshold
exceeded,
trigger
oxidative
damage,
ultimately
leading
cell
death.
Based
on
this,
metabolic
functions
generation
considered
attractive
targets
synthetic
natural
anticancer
compounds.
Tocotrienols
(TTs),
specifically
δ-
γ-TT
isoforms,
vitamin
E-derived
biomolecules
widely
shown
possess
striking
properties
since
they
regulate
several
molecular
pathways.
Herein,
we
provide
for
first
time
an
overview
reprogramming
redox
homeostasis
perturbation
occurring
cells,
highlighting
involvement
TTs.
This
sheds
light
use
these
compounds
promising
preventive
or
therapeutic
approach
novel
strategies.