p53-regulated non-apoptotic cell death pathways and their relevance in cancer and other diseases
Nature Reviews Molecular Cell Biology,
Год журнала:
2025,
Номер
unknown
Опубликована: Апрель 9, 2025
Язык: Английский
Crosstalk between inflammasome sensors and DNA damage response pathways
FEBS Journal,
Год журнала:
2024,
Номер
unknown
Опубликована: Янв. 25, 2024
Eukaryotic
cells
encounter
diverse
threats
jeopardizing
their
integrity,
prompting
the
development
of
defense
mechanisms
against
these
stressors.
Among
mechanisms,
inflammasomes
are
well‐known
for
roles
in
coordinating
inflammatory
response
infections.
Extensive
research
has
unveiled
multifaceted
involvement
cellular
processes
beyond
inflammation.
Recent
studies
emphasize
intricate
relationship
between
inflammasome
and
DNA
damage
(DDR).
They
highlight
how
DDR
participates
activation
reciprocal
impact
on
genome
integrity
preservation.
Moreover,
novel
functions
sensors
pathways
have
emerged,
broadening
our
understanding
roles.
Finally,
this
review
delves
into
identifying
common
signals
that
drive
alongside
cues
response,
offering
potential
insights
shared
regulatory
critical
processes.
Язык: Английский
Role of Lipopolysaccharides in the Inflammation and Pyroptosis of Alveolar Epithelial Cells in Acute Lung Injury and Acute Respiratory Distress Syndrome
Journal of Inflammation Research,
Год журнала:
2024,
Номер
Volume 17, С. 5855 - 5869
Опубликована: Авг. 1, 2024
Acute
lung
injury
(ALI)
and
acute
respiratory
distress
syndrome
(ARDS)
represent
a
spectrum
of
common
critical
conditions
characterized
by
damage
death
alveolar
epithelial
cells
(AECs).
Pyroptosis
is
form
programmed
cell
with
inflammatory
characteristics,
activation
pyroptosis
markers
has
been
observed
in
AECs
patients
ALI/ARDS.
Lipopolysaccharides
(LPS)
possess
strong
pro-inflammatory
effects
are
crucial
pathological
factor
leading
to
ALI
animals.
In
LPS-induced
models,
undergo
pyroptosis.
However,
physiologically
pathologically
relevant
concentrations
LPS
lead
minor
on
AEC
viability
minimal
induction
cytokine
release
vitro
do
not
induce
classical
Nevertheless,
can
enter
the
cytoplasm
directly
non-classical
when
assisted
extracellular
vesicles
from
bacteria,
HMGB1,
pathogens.
this
review,
we
have
explored
concerning
inflammation,
viability,
pyroptosis,
analyzing
key
factors
that
influence
actions.
Notably,
highlight
intricate
response
within
framework
ARDS,
emphasizing
variable
Despite
vitro,
under
specific
conditions,
presenting
potential
pathways
for
therapeutic
intervention.
Collectively,
understanding
these
mechanisms
development
targeted
treatments
mitigate
responses
ALI/ARDS,
thereby
enhancing
patient
outcomes
severe
conditions.
Язык: Английский
Inflammasome protein scaffolds the DNA damage complex during tumor development
Nature Immunology,
Год журнала:
2024,
Номер
25(11), С. 2085 - 2096
Опубликована: Окт. 14, 2024
Язык: Английский
The Co-Localization of NLRP3 and ASC Specks Does Not Automatically Entail NLRP3 Inflammasome Functionality in PDAC Cell Lines
International Journal of Translational Medicine,
Год журнала:
2024,
Номер
4(2), С. 224 - 237
Опубликована: Март 30, 2024
The
NLRP3
inflammasome
is
an
important
mediator
of
the
host
inflammatory
response,
and
downregulation
inflammation
in
cancer
treatment.
Here,
we
investigated
four
different
pancreatic
ductal
adenocarcinoma
(PDAC)
cell
lines,
AsPC-1,
BxPC-3,
CFPAC-1
Panc-1,
with
regards
to
formation
cytokine
secretion.
ASC
specks
were
observed
all
lines
investigated,
but
AsPC-1
was
only
cell-line
co-localization
anti-ASC
anti-NLRP3
spontaneously
formed
multiple
inflammasomes
per
cell.
not
accompanied
by
IL-1β
release
nor
significant
IL-18
release.
BxPC-3
displayed
relatively
high
expression
inflammasome-related
genes
IL1B
CASP1
had
highest
levels
IL1β
IL18
secretion
amount
ASC.
inflammasome-associated
PYCARD
up-regulated
PDAC
primary
tumors
compared
normal
tissue,
tumor
IL18,
correlated
low
patient
survival.
We
have
shown
that
display
variations
their
gene
readouts.
conclude
spontaneous
speck
possible
cells
are
does
automatically
entail
function.
Язык: Английский
The inflammasome sensor NLRP3 interacts with REV7 to maintain genome integrity through homologous recombination
Delphine Burlet,
Md. Muntaz Khan,
Sabine Hacot
и другие.
bioRxiv (Cold Spring Harbor Laboratory),
Год журнала:
2024,
Номер
unknown
Опубликована: Ноя. 28, 2024
ABSTRACT
DNA
double
strand
break
(DSB)
is
a
highly
toxic
lesion
that
can
generate
genome
instability,
major
source
of
tumorigenesis.
DSBs
are
mainly
repaired
by
non-homologous
end
joining
(NHEJ)
or
homologous
recombination
(HR).
The
selection
the
DSB
repair
pathway
primarily
depends
on
resection
ends.
Indeed,
HR
initiated
at
generating
3’
single
stranded
extension.
shieldin
complex
prevents
fostering
toward
NHEJ.
Here,
we
reveal
inflammasome
sensor
NLRP3
facilitates
to
promote
in
an
inflammasome-independent
manner.
Strikingly,
silencing
decreases
efficiency,
as
evidenced
RAD51
foci
and
functional
assays.
Mechanistically,
describe
interacts
with
REV7,
subunit
complex,
its
depletion
increases
REV7
recruitment
IR-induced
DSBs.
Similar
cancer
cells
harboring
mutated
genes,
find
deficient
sensitive
PARP
inhibitors
(PARPi)
exhibit
epistatic
relationship
BRCA1
deficiency.
Remarkably,
loss
NLRP3-depleted
induces
PARPi
resistance
restoring
HR.
This
study
unravels
crucial
role
innate
immune
receptor
regulating
pathways
maintain
integrity.
Язык: Английский