World Journal of Stem Cells,
Год журнала:
2024,
Номер
16(8), С. 773 - 779
Опубликована: Авг. 26, 2024
In
this
editorial,
we
delved
into
the
article
titled
“Cellular
preconditioning
and
mesenchymal
stem
cell
ferroptosis.”
This
groundbreaking
study
underscores
a
pivotal
discovery:
Ferroptosis,
type
of
programmed
death,
drastically
reduces
viability
donor
cells
(MSCs)
after
engraftment,
thereby
undermining
therapeutic
value
cell-based
therapies.
Furthermore,
proposes
that
by
manipulating
ferroptosis
mechanisms
through
preconditioning,
can
potentially
enhance
survival
rate
functionality
MSCs,
ultimately
amplifying
their
potential.
Given
crucial
role
plays
in
shaping
outcomes
deem
it
imperative
to
further
investigate
intricate
interplay
between
death
effectiveness
MSCs.
Abstract
Pyroptosis
possesses
potent
antitumor
immune
activity,
making
pyroptosis
inducer
development
a
promising
direction
for
tumor
immunotherapy.
Persistent
luminescence
nanoparticles
(PLNPs)
are
highly
sensitive
optical
probes
extensively
employed
in
diagnosis
and
therapy.
However,
based
on
PLNPs
has
not
been
reported
yet.
Herein,
polyethylene
glycol–poly
lactic
acid‐co‐glycolic
acid
(PEG–PLGA:
PP)
modified
biodegradable
CaS:Eu
2+
(CSE@PP)
synthesized
as
immunotherapy
the
first
time.
The
CSE@PP
biowindow
persistent
(PersL)
pH‐responsive
degradation
properties,
allowing
it
to
remain
stable
under
neutral
pH
but
degrade
when
exposed
weak
(pH
<
6.5).
During
within
tumor,
constantly
releases
H
2
S
Ca
while
its
PersL
gradually
fades
away.
Thus,
signal
can
self‐monitor
release.
Furthermore,
released
result
mitochondrial
dysfunction
inactivation
of
reactive
oxygen
species
scavenging
enzymes,
synergistic
facilitating
intracellular
oxidative
stress,
which
induces
caspase‐1/GSDM‐D
dependent
subsequent
responses.
In
word,
is
confirmed
that
release
pyroptosis‐mediated
Immunotherapy.
This
work
will
facilitate
biomedical
applications
inspire
pyroptosis‐induced
Toxics,
Год журнала:
2025,
Номер
13(1), С. 41 - 41
Опубликована: Янв. 7, 2025
Acrylamide
(ACR)
is
a
commonly
used
organic
compound
that
exhibits
evident
neurotoxicity
in
humans.
Our
previous
studies
showed
the
mechanisms
of
ACR-caused
included
apoptosis,
PERK-mediated
endoplasmic
reticulum
stress,
and
autophagy,
but
relationships
among
them
were
still
unclear.
This
paper
investigated
PERK
pathway
to
demonstrate
mechanism
ACR
further.
Different
doses
set
value
toxicity.
Then,
inhibitor
autophagy
inhibitor,
GSK2606414
3-methyladenine
(3-MA),
separately
inhibit
activation
SH-SY5Y
cells
under
treatment.
With
increase
dose,
apoptotic
rate
increased
dose-dependent
manner.
After
inhibition
pathway,
activated
apoptosis
autophagosome
accumulation
caused
by
alleviated.
Under
3-MA
treatment,
deteriorated
had
no
significant
effect
on
ACR-induced
activation;
thus,
pathway-induced
an
antiapoptotic
role
this
condition.
provides
experimental
basis
for
exploring
potential
molecular
targets
prevent
control
Cancer-associated
fibroblasts
(CAFs)
are
key
components
of
tumor
microenvironment
and
have
been
identified
to
be
involved
in
modulating
drug
resistance
cancers
by
secreting
molecules.
Pancreatic
cancer
(PC)
is
a
leading
cause
mortality
with
high
aggressiveness.
Gemcitabine
(GEM)
one
primary
antineoplastic
drugs
for
PC.
Collagen
XVII
(COL17A1)
expression
was
found
upregulated
GEM-resistant
CAFs.
Here,
this
study
focused
on
investigating
whether
CAFs
affected
GEM
PC
COL17A1
its
associated
mechanisms.
In
total,
60
newly
diagnosed
patients
only
GEM-based
chemotherapy
were
recruited.
Normal
(NFs)
isolated
using
fresh
normal
resistant
tissues.
Human
pancreatic
duct
epithelial
(HPDE)
cells
used
functional
analyses.
Levels
Actinin
Alpha
4
(ACTN4)
measured
qRT-PCR
western
blotting.
Functional
analyses
conducted
MTT,
5-ethynyl-2ʹ-deoxyuridine,
transwell,
sphere
formation
assays,
respectively.
The
interaction
between
ACTN4
analyzed
Co-immunoprecipitation
immunofluorescence
assays.
Animal
models
established
vivo
analysis.
CAF
incubation
promoted
enhanced
the
proliferation,
invasion
stemness
cells.
highly
expressed
cells,
could
increase
Moreover,
silencing
or
COL17A1-decreased
suppress
cell
oncogenic
phenotype
progression.
Mechanistically,
interacted
protein,
anticancer
effects
mediated
reversed
overexpression.
assay
also
showed
that
suppressed
growth
ACTN4.
CAFs-derived
tumorigenesis
interacting
ACTN4,
suggesting
new
method
overcoming
Scientific Reports,
Год журнала:
2025,
Номер
15(1)
Опубликована: Фев. 27, 2025
Carcinoma-associated
fibroblasts
(CAFs)
exhibit
significant
heterogeneity
and
are
closely
associated
with
progression,
resistance
to
anticancer
therapies,
poor
prognosis
in
head
neck
squamous
cell
carcinoma
(HNSCC).
However,
the
specific
functional
role
of
CAFs
HNSCC
has
been
inadequately
explored.
In
this
study,
we
utilized
a
single-cell
RNA
sequencing
dataset
from
(GSE103322)
recluster
via
Seurat
pipeline.
On
basis
reported
markers,
identified
two
CAF
subtypes,
LOX-myCAFs
LOX
+
iCAFs,
generated
signature
markers
for
each.
Through
unsupervised
consensus
clustering,
characterized
molecular
subtypes
HNSCC-TCGA,
each
exhibiting
distinct
dysregulated
cancer
hallmarks,
immunological
tumor
microenvironments,
stemness
characteristics.
The
robustness
iCAF-related
particularly
terms
prediction
immunotherapeutic
response,
was
validated
an
ANOVA
cohort
GEO
(GSE159067)
consisting
102
patients.
A
positive
correlation
between
expression
that
CD86,
marker
M1
macrophage
polarization.
Further
experiments
involving
coculture
conditioned
medium
derived
LOX-silenced
CAL-27
UM-SCC-1
lines
revealed
silencing
led
decreased
proliferation
migration
these
cells,
which
mediated
by
epithelial-mesenchymal
transition
(EMT)
through
IL-34-
induced
CSF1R/Akt
signaling.
summary,
our
bulk
analyses
can
predict
response
immunotherapy
Additionally,
gene
as
promising
therapeutic
target
treatment.
Metabolites,
Год журнала:
2025,
Номер
15(3), С. 201 - 201
Опубликована: Март 13, 2025
Background:
Tumor
cells
engage
in
continuous
self-replication
by
utilizing
a
large
number
of
resources
and
capabilities,
typically
within
an
aberrant
metabolic
regulatory
network
to
meet
their
own
demands.
This
dysregulation
leads
the
formation
tumor
microenvironment
(TME)
most
solid
tumors.
Nanomedicines,
due
unique
physicochemical
properties,
can
achieve
passive
targeting
certain
tumors
through
enhanced
permeability
retention
(EPR)
effect,
or
active
deliberate
design
optimization,
resulting
accumulation
TME.
The
use
nanomedicines
target
critical
pathways
holds
significant
promise.
However,
requires
careful
selection
relevant
drugs
materials,
taking
into
account
multiple
factors.
traditional
trial-and-error
process
is
relatively
inefficient.
Artificial
intelligence
(AI)
integrate
big
data
evaluate
delivery
efficiency
nanomedicines,
thereby
assisting
nanodrugs.
Methods:
We
have
conducted
detailed
review
key
papers
from
databases,
such
as
ScienceDirect,
Scopus,
Wiley,
Web
Science,
PubMed,
focusing
on
reprogramming,
mechanisms
action
development
metabolism,
application
AI
empowering
nanomedicines.
integrated
content
present
current
status
research
metabolism
potential
future
directions
this
field.
Results:
Nanomedicines
possess
excellent
TME
which
be
utilized
disrupt
cells,
including
glycolysis,
lipid
amino
acid
nucleotide
metabolism.
disruption
selective
killing
disturbance
Extensive
has
demonstrated
that
AI-driven
methodologies
revolutionized
nanomedicine
development,
while
concurrently
enabling
precise
identification
molecular
regulators
involved
oncogenic
reprogramming
pathways,
catalyzing
transformative
innovations
targeted
cancer
therapeutics.
Conclusions:
great
Additionally,
will
accelerate
discovery
metabolism-related
targets,
empower
optimization
help
minimize
toxicity,
providing
new
paradigm
for
development.
