Cancer Cell International,
Год журнала:
2025,
Номер
25(1)
Опубликована: Фев. 25, 2025
α5-nicotinic
acetylcholine
receptor
(α5‐nAChR)
participates
in
chronic
stress-promoted
lung
adenocarcinoma
(LUAD)
progression.
Neuropilin
and
tolloid-like
2
(NETO2)
contributes
to
fear
expression
extinction,
which
is
related
tumorigenesis.
CHRNA5
(encoding
α5‐nAChR)
gene
profiling
revealed
a
reduction
NETO2
following
knockdown.
Nevertheless,
the
connection
between
α5-nAChR
LUAD
progression
induced
by
stress
remains
unclear.
RNA-Seq
bioinformatics
database
were
used
for
analyzing
as
well
correlation
of
α5-nAChR,
together
with
LUAD.
detected
using
immunohistochemistry
tissue
microarrays,
restraint
(CRS)
unpredictable
(CUMS)
mice
tissues.
In
A549
H1299
cells,
NETO2,
p-CAMKII,
p-STAT3
vimentin
acetylcholine/nicotine
was
examined
western
blot.
The
interaction
cells
Co-immunoprecipitation
assay
modeled
molecular
docking.
EdU
colony
formation
conducted
evaluate
cell
proliferation,
while
wound
healing
transwell
assessed
migration
invasion
cells.
expression,
low
survival
rate,
staging
smoking
status
dataset
microarrays.
validated
nude
xenograft
correlated
CRS
CUMS
vitro,
mediated
via
α5-nAChR.
interacted
CAMKII
α5-nAChR/NETO2
signaling
contributed
invasion.
above
results
uncover
new
pathway:
axis
Cancer and Metastasis Reviews,
Год журнала:
2025,
Номер
44(1)
Опубликована: Янв. 20, 2025
Nerve
signaling
within
the
tumor
microenvironment
(TME)
plays
a
critical
role
in
initiation,
progression,
and
metastasis
of
solid
tumors.
Due
to
their
highly
responsive
behavior
activation
upon
injury
cancer
onset,
this
review
specifically
focuses
on
how
sympathetic
nerves
rewire
TME.
Within
tumors,
closely
interact
with
various
TME
components,
combined
often
shifts
tumor-intrinsic
physiology
toward
tumor-supportive
phenotypes.
In
turn,
such
as
myeloid
cells,
lymphoid
extracellular
matrix
(ECM),
endothelial
associated
fibroblasts
(CAFs),
Schwann
secrete
neurotrophic
axon
guidance
factors
that
influence
both
outgrowth
cell
behavior,
further
exacerbating
progression
metastasis.
Here,
we
current
evidence
multidirectional
impacts
immune
non-immune
nature
these
communication
processes,
exploring
interactions
may
inform
future
therapeutics
impair
Abstract
Aging
is
an
inevitable
physiological
process
in
organisms,
and
the
development
of
tumors
closely
associated
with
cellular
senescence.
This
article
initially
examines
role
senescence
tumorigenesis,
emphasizing
correlation
between
telomere
length—a
marker
senescence—and
tumor
risk.
Concurrently,
study
explores
expression
levels
senescence-associated
markers,
such
as
p16,
p53,
mTOR,
context
development.
Additionally,
investigates
impact
on
organismal
senescence,
including
effects
immune
system
function
metabolic
processes.
Ultimately,
discussion
potential
application
anti-aging
strategies
therapy
considers
possibility
utilizing
mechanisms
a
novel
therapeutic
approach
for
tumors.
research
provides
insights
into
complex
interplay
development,
suggesting
future
preventative
measures
interventions.
International Journal of Molecular Sciences,
Год журнала:
2025,
Номер
26(4), С. 1493 - 1493
Опубликована: Фев. 11, 2025
(1)
Liver
injury
caused
by
an
overdose
of
acetaminophen
(APAP)
represents
a
major
public
health
concern.
Paeoniflorin
(PF)
has
been
reported
to
have
anti-inflammatory
and
liver-protective
effects,
but
the
underlying
mechanisms
remain
unclear.
This
study
aimed
investigate
effect
PF
on
crosstalk
between
pyroptosis
NETs
in
AILI.
(2)
APAP-treated
C57BL/6J
mice
were
used
demonstrate
protective
liver
injury.
HepG2
dHL-60
cells
cultured
effects
hepatocyte
neutrophil
extracellular
traps
(NETs)
vitro.
Moreover,
cell
co-culture
experiments
performed,
treated
with
NETs-depleting
agent
inhibitor
improvement
AILI
induced
through
regulating
NETs.
(3)
significantly
alleviated
Additionally,
inhibited
expression
pyroptosis-related
proteins,
high-mobility
group
box
1
(HMGB1),
NETs-associated
proteins
vitro
vivo.
The
demonstrated
that
not
only
triggered
pyroptosis,
also
suppressed
In
depleted
neutrophils,
level
notably
decreased,
indicating
diminished
impact
PF.
Similarly,
formation
was
reduced
receiving
compared
APAP
group.
Compared
DNase
I
alone,
reduction
combined
serum
ALT
AST
levels
decreased
from
46.857%
39.927%
44.347%
33.419%,
respectively.
DSF
45.347%
36.419%,
(4)
therapeutic
Its
mechanism
involves
regulation
research
substantiates
pharmacological
promise
as
intervention
for
acute
Cancer Cell International,
Год журнала:
2025,
Номер
25(1)
Опубликована: Фев. 25, 2025
α5-nicotinic
acetylcholine
receptor
(α5‐nAChR)
participates
in
chronic
stress-promoted
lung
adenocarcinoma
(LUAD)
progression.
Neuropilin
and
tolloid-like
2
(NETO2)
contributes
to
fear
expression
extinction,
which
is
related
tumorigenesis.
CHRNA5
(encoding
α5‐nAChR)
gene
profiling
revealed
a
reduction
NETO2
following
knockdown.
Nevertheless,
the
connection
between
α5-nAChR
LUAD
progression
induced
by
stress
remains
unclear.
RNA-Seq
bioinformatics
database
were
used
for
analyzing
as
well
correlation
of
α5-nAChR,
together
with
LUAD.
detected
using
immunohistochemistry
tissue
microarrays,
restraint
(CRS)
unpredictable
(CUMS)
mice
tissues.
In
A549
H1299
cells,
NETO2,
p-CAMKII,
p-STAT3
vimentin
acetylcholine/nicotine
was
examined
western
blot.
The
interaction
cells
Co-immunoprecipitation
assay
modeled
molecular
docking.
EdU
colony
formation
conducted
evaluate
cell
proliferation,
while
wound
healing
transwell
assessed
migration
invasion
cells.
expression,
low
survival
rate,
staging
smoking
status
dataset
microarrays.
validated
nude
xenograft
correlated
CRS
CUMS
vitro,
mediated
via
α5-nAChR.
interacted
CAMKII
α5-nAChR/NETO2
signaling
contributed
invasion.
above
results
uncover
new
pathway:
axis
