Advances in non-apoptotic regulated cell death: implications for malignant tumor treatment
Frontiers in Oncology,
Год журнала:
2025,
Номер
15
Опубликована: Янв. 30, 2025
Cell
death
mechanisms
are
broadly
classified
into
accidental
cell
(ACD)
and
regulated
(RCD).
ACD
such
as
necrosis,
is
an
uncontrolled,
process,
while
RCD
tightly
by
specific
signaling
pathways
molecular
mechanisms.
Tumor
cells
characterized
their
ability
to
evade
sustain
uncontrolled
proliferation.
The
failure
of
programmed
a
key
contributor
tumor
initiation,
progression,
resistance
cancer
therapies.
Traditionally,
research
has
focused
primarily
on
apoptosis
the
dominant
form
in
cancer.
However,
emerging
evidence
highlights
importance
other
non-apoptotic
forms
RCD,
pyroptosis,
ferroptosis,
necroptosis,
parthanatos,
tumorigenesis
treatment
response.
These
gaining
attention
for
potential
roles
overcoming
therapy
resistance.
In
this
review,
we
will
discuss
recent
advances
study
malignant
tumors
explore
therapeutic
implications,
offering
insights
new
targets
strategies.
Язык: Английский
New hope for the world cancer day
Biology Direct,
Год журнала:
2025,
Номер
20(1)
Опубликована: Фев. 4, 2025
Язык: Английский
ALDH1A3 Regulates Cellular Senescence and Senescence-Associated Secretome in Prostate Cancer
Cancers,
Год журнала:
2025,
Номер
17(7), С. 1184 - 1184
Опубликована: Март 31, 2025
Background:
Radiotherapy
is
a
key
treatment
for
cancer,
effectively
controlling
local
tumor
growth
through
DNA
damage
that
induces
senescence
or
apoptosis
in
cancer
cells.
However,
radiotherapy
can
trigger
complex
cellular
reactions,
such
as
cell
senescence,
which
characterized
by
irreversible
cycle
arrest
and
the
secretion
of
pro-inflammatory
factors
known
senescent-associated
secretory
phenotype
(SASP).
Methods:
This
study
investigates
regulatory
role
ALDH1A3,
enzyme
implicated
metabolism
resistance,
induction
SASP.
Using
vitro
models,
we
demonstrate
ALDH1A3
knockdown
accelerates
senescent-like
while
regulating
SASP
cGAS-STING
immune
response
pathway.
Results:
Our
results
indicate
promotes
it
reduces
via
inhibition
pathway,
potentially
mitigating
SASP-related
progression.
Conclusions:
These
findings
provide
insights
into
molecular
mechanisms
underlying
prostate
suggest
could
be
potential
therapeutic
target
to
enhance
efficacy
adverse
effects
Язык: Английский
IL-1β+ macrophages and the control of pathogenic inflammation in cancer
Trends in Immunology,
Год журнала:
2025,
Номер
unknown
Опубликована: Март 1, 2025
Язык: Английский
Cell death, IL-1 cytokines, and tumor progression
Cancer Cell,
Год журнала:
2025,
Номер
unknown
Опубликована: Апрель 1, 2025
Язык: Английский
Antimitotic chemotherapy promotes tumor NF-kB secretory phenotype and immunosuppressive CXCR2+ neutrophils chemotaxis in triple-negative breast cancers
bioRxiv (Cold Spring Harbor Laboratory),
Год журнала:
2024,
Номер
unknown
Опубликована: Дек. 23, 2024
ABSTRACT
Integrated
approaches
that
help
understand
how
tumors,
as
immune-surveilled
ecosystems,
respond
to
chemotherapy
are
crucial
for
developing
effective
antitumor
treatments.
We
previously
showed,
in
immunodeficient
context,
antimitotic
induced
cGAS/STING
pathway
amplifying
response
through
a
paracrine
IFN-1
secretome.
herein
studied
tumor
progression
and
treatment
using
an
immunocompetent
murine
model.
scRNAseq
analysis
revealed
paclitaxel
altered
cell
phenotypes,
favoring
cells
with
gene
expression
signature
indicative
of
active
NF-κB
secretory
phenotype.
Treatment
coincidently
reduced
IFN-I
during
progression.
The
resulting
shift
correlated
neutrophil
recruitment
the
tumor,
particularly
CXCR2+
neutrophils,
thereby
contributing
immunosuppressive
microenvironment.
Pharmacological
inhibition
CXCR2
receptor
by
navarixin
reactivated
immunity,
enhancing
NK
infiltration
cytotoxicity.
Navarixin
combination
significantly
volume
metastasis.
Targeting
NF-κB-driven
phenotype,
particular
modulation,
holds
promise
improving
TNBC
outcomes.
Язык: Английский