Cell Death Discovery,
Год журнала:
2023,
Номер
9(1)
Опубликована: Апрель 1, 2023
Lung
cancer
is
a
common
malignant
tumor
that
occurs
in
the
human
body
and
poses
serious
threat
to
health
quality
of
life.
The
existing
treatment
methods
mainly
include
surgical
treatment,
chemotherapy,
radiotherapy.
However,
due
strong
metastatic
characteristics
lung
emergence
related
drug
resistance
radiation
resistance,
overall
survival
rate
patients
not
ideal.
There
an
urgent
need
develop
new
strategies
or
effective
drugs
treat
cancer.
Ferroptosis,
novel
type
programmed
cell
death,
different
from
traditional
death
pathways
such
as
apoptosis,
necrosis,
pyroptosis
so
on.
It
caused
by
increase
iron-dependent
reactive
oxygen
species
intracellular
iron
overload,
which
leads
accumulation
lipid
peroxides,
thus
inducing
membrane
oxidative
damage,
affecting
normal
life
process
cells,
finally
promoting
ferroptosis.
regulation
ferroptosis
closely
physiological
it
involves
metabolism,
balance
between
oxygen-free
radical
reaction
peroxidation.
A
large
number
studies
have
confirmed
result
combined
action
cellular
oxidation/antioxidant
system
damage/repair,
has
great
potential
application
therapy.
Therefore,
this
review
aims
explore
therapeutic
targets
for
clarifying
regulatory
pathway
Based
on
study
ferroptosis,
mechanism
was
understood
chemical
natural
compounds
targeting
were
summarized,
with
aim
providing
ideas
In
addition,
also
provides
basis
discovery
clinical
effectively
International Journal of Molecular Sciences,
Год журнала:
2022,
Номер
24(1), С. 449 - 449
Опубликована: Дек. 27, 2022
Regulated
cell
death
(RCD)
has
a
significant
impact
on
development,
tissue
homeostasis,
and
the
occurrence
of
various
diseases.
Among
different
forms
RCD,
ferroptosis
is
considered
as
type
reactive
oxygen
species
(ROS)-dependent
regulated
necrosis.
ROS
can
react
with
polyunsaturated
fatty
acids
(PUFAs)
lipid
(L)
membrane
via
formation
radical
L•
induce
peroxidation
to
form
L-ROS.
Ferroptosis
triggered
by
an
imbalance
between
hydroperoxide
(LOOH)
detoxification
iron-dependent
L-ROS
accumulation.
Intracellular
iron
accumulation
are
two
central
biochemical
events
leading
ferroptosis.
Organelles,
including
mitochondria
lysosomes
involved
in
regulation
metabolism
redox
In
this
review,
we
will
provide
overview
peroxidation,
well
key
components
ferroptotic
cascade.
The
main
mechanism
that
reduces
ability
glutathione
(GSH).
GSH,
tripeptide
includes
glutamic
acid,
cysteine,
glycine,
acts
antioxidant
substrate
peroxidase
4
(GPX4),
which
then
converted
into
oxidized
(GSSG).
Increasing
expression
GSH
inhibit
We
highlight
role
xc-
GSH-GPX4
pathway
regulate
system
xc-,
composed
subunit
solute
carrier
family
members
(SLC7A11
SLC3A2),
mediates
exchange
cystine
glutamate
across
plasma
synthesize
GSH.
Accumulating
evidence
indicates
requires
autophagy
machinery
for
its
execution.
Ferritinophagy
used
describe
removal
major
storage
protein
ferritin
machinery.
Nuclear
receptor
coactivator
(NCOA4)
cytosolic
bind
subsequent
degradation
ferritinophagy.
During
ferritinophagy,
stored
released
becomes
available
biosynthetic
pathways.
dysfunctional
response
implicated
variety
pathological
conditions.
inducers
or
inhibitors
targeting
redox-
metabolism-related
proteins
signal
transduction
have
been
developed.
simultaneous
detection
intracellular
extracellular
markers
may
help
diagnose
treat
diseases
related
damage.
Frontiers in Pharmacology,
Год журнала:
2022,
Номер
13
Опубликована: Авг. 29, 2022
The
activation
of
ferroptosis
is
a
new
effective
way
to
treat
drug-resistant
solid
tumors.
Ferroptosis
an
iron-mediated
form
cell
death
caused
by
the
accumulation
lipid
peroxides.
intracellular
imbalance
between
oxidant
and
antioxidant
due
abnormal
expression
multiple
redox
active
enzymes
will
promote
produce
reactive
oxygen
species
(ROS).
So
far,
few
pathways
regulators
have
been
discovered
regulate
ferroptosis.
In
particular,
cystine/glutamate
antiporter
(System
X
c
−
),
glutathione
peroxidase
4
(GPX4)
(GSH)
/GSH/GPX4
axis)
plays
key
role
in
preventing
peroxidation-mediated
ferroptosis,
because
which
could
be
inhibited
blocking
System
axis.
This
review
aims
present
current
understanding
mechanism
based
on
axis
treatment
Abstract
Background
Cancer
is
the
most
prevalent
cause
of
death
globally,
and
radiotherapy
considered
standard
care
for
solid
tumors,
including
lung,
breast,
esophageal,
colorectal
cancers
glioblastoma.
Resistance
to
radiation
can
lead
local
treatment
failure
even
cancer
recurrence.
Main
body
In
this
review,
we
have
extensively
discussed
several
crucial
aspects
that
resistance
therapy,
radiation-induced
DNA
damage
repair,
cell
cycle
arrest,
apoptosis
escape,
abundance
stem
cells,
modification
cells
their
microenvironment,
presence
exosomal
non-coding
RNA,
metabolic
reprogramming,
ferroptosis.
We
aim
focus
on
molecular
mechanisms
in
relation
these
discuss
possible
targets
improve
outcomes.
Conclusions
Studying
responsible
its
interactions
with
tumor
environment
will
help
responses
radiotherapy.
Our
review
provides
a
foundation
identify
overcome
obstacles
effective
Signal Transduction and Targeted Therapy,
Год журнала:
2024,
Номер
9(1)
Опубликована: Март 8, 2024
Ferroptosis
is
a
non-apoptotic
form
of
regulated
cell
death
characterized
by
the
lethal
accumulation
iron-dependent
membrane-localized
lipid
peroxides.
It
acts
as
an
innate
tumor
suppressor
mechanism
and
participates
in
biological
processes
tumors.
Intriguingly,
mesenchymal
dedifferentiated
cancer
cells,
which
are
usually
resistant
to
apoptosis
traditional
therapies,
exquisitely
vulnerable
ferroptosis,
further
underscoring
its
potential
treatment
approach
for
cancers,
especially
refractory
cancers.
However,
impact
ferroptosis
on
extends
beyond
direct
cytotoxic
effect
cells.
induction
not
only
inhibits
but
also
promotes
development
due
negative
anticancer
immunity.
Thus,
comprehensive
understanding
role
crucial
successful
translation
therapy
from
laboratory
clinical
applications.
In
this
review,
we
provide
overview
recent
advancements
cancer,
covering
molecular
mechanisms,
functions,
regulatory
pathways,
interactions
with
microenvironment.
We
summarize
applications
immunotherapy,
radiotherapy,
systemic
therapy,
well
inhibition
various
conditions.
finally
discuss
markers,
current
challenges
future
directions
cancer.
Journal of Hematology & Oncology,
Год журнала:
2023,
Номер
16(1)
Опубликована: Июль 25, 2023
Abstract
Tumour-associated
macrophages
(TAMs)
are
crucial
components
of
the
tumour
microenvironment
and
play
a
significant
role
in
development
drug
resistance
by
creating
an
immunosuppressive
microenvironment.
Macrophages
essential
both
innate
adaptive
immune
systems
contribute
to
pathogen
regulation
organism
homeostasis.
Macrophage
function
polarization
closely
linked
altered
metabolism.
Generally,
M1
rely
primarily
on
aerobic
glycolysis,
whereas
M2
depend
oxidative
Metabolic
studies
have
revealed
that
metabolic
signature
TAMs
metabolites
regulate
TAMs.
However,
precise
effects
reprogramming
tumours
remain
incompletely
understood.
In
this
review,
we
discuss
impact
pathways
macrophage
as
well
potential
strategies
for
metabolism
cancer
treatment.
Nature Communications,
Год журнала:
2023,
Номер
14(1)
Опубликована: Июнь 21, 2023
The
cystine
transporter
solute
carrier
family
7
member
11
(SLC7A11;
also
called
xCT)
protects
cancer
cells
from
oxidative
stress
and
is
overexpressed
in
many
cancers.
Here
we
report
a
surprising
finding
that,
whereas
moderate
overexpression
of
SLC7A11
beneficial
for
treated
with
H2O2,
common
inducer,
its
high
dramatically
increases
H2O2-induced
cell
death.
Mechanistically,
uptake
combination
H2O2
treatment
results
toxic
buildup
intracellular
other
disulfide
molecules,
NADPH
depletion,
redox
system
collapse,
rapid
death
(likely
disulfidptosis).
We
further
show
that
promotes
tumor
growth
but
suppresses
metastasis,
likely
because
metastasizing
expression
are
particularly
susceptible
to
stress.
Our
findings
reveal
level
dictates
cells'
sensitivity
suggests
context-dependent
role
biology.
