Molecular Therapy,
Journal Year:
2021,
Volume and Issue:
29(7), P. 2185 - 2208
Published: March 30, 2021
Ferroptosis
is
an
iron-
and
lipid
reactive
oxygen
species
(ROS)-dependent
form
of
programmed
cell
death
that
distinct
from
other
forms
regulatory
at
the
morphological,
biological,
genetic
levels.
Emerging
evidence
suggests
critical
roles
for
ferroptosis
in
metabolism,
redox
status,
various
diseases,
such
as
cancers,
nervous
system
ischemia-reperfusion
injury,
with
ferroptosis-related
proteins.
inhibited
diverse
cancer
types
functions
a
dynamic
tumor
suppressor
development,
indicating
regulation
can
be
utilized
interventional
target
treatment.
Small
molecules
nanomaterials
reprogram
cells
to
undergo
are
considered
effective
drugs
therapy.
Here,
we
systematically
summarize
molecular
basis
ferroptosis,
suppressive
effect
on
tumors,
cellular
metabolism
microenvironment
(TME),
ferroptosis-inducing
agents
therapeutics.
An
understanding
latest
progress
could
provide
references
proposing
new
potential
targets
treatment
cancers.
Cell Death and Disease,
Journal Year:
2020,
Volume and Issue:
11(2)
Published: Feb. 3, 2020
Abstract
Ferroptosis
is
a
new
type
of
cell
death
that
was
discovered
in
recent
years
and
usually
accompanied
by
large
amount
iron
accumulation
lipid
peroxidation
during
the
process;
occurrence
ferroptosis
iron-dependent.
Ferroptosis-inducing
factors
can
directly
or
indirectly
affect
glutathione
peroxidase
through
different
pathways,
resulting
decrease
antioxidant
capacity
reactive
oxygen
species
(ROS)
cells,
ultimately
leading
to
oxidative
death.
Recent
studies
have
shown
closely
related
pathophysiological
processes
many
diseases,
such
as
tumors,
nervous
system
ischemia-reperfusion
injury,
kidney
blood
diseases.
How
intervene
development
diseases
regulating
has
become
hotspot
focus
etiological
research
treatment,
but
functional
changes
specific
molecular
mechanisms
still
need
be
further
explored.
This
paper
systematically
summarizes
latest
progress
research,
with
on
providing
references
for
understanding
its
pathogenesis
proposing
targets
treatment
Journal of Hematology & Oncology,
Journal Year:
2019,
Volume and Issue:
12(1)
Published: March 29, 2019
Ferroptosis
is
a
novel
type
of
cell
death
with
distinct
properties
and
recognizing
functions
involved
in
physical
conditions
or
various
diseases
including
cancers.
The
fast-growing
studies
ferroptosis
cancer
have
boosted
perspective
for
its
usage
therapeutics.
Here,
we
review
the
current
findings
regulation
especially
focus
on
function
ncRNAs
mediating
process
ferroptotic
how
was
relation
to
other
regulated
deaths.
Aberrant
diverse
types
tissues
were
summarized,
elaborated
recent
data
about
actors
some
"conventional"
drugs
natural
compounds
as
inducers
cancer.
Finally,
deliberate
future
orientation
cells
unsettled
issues,
which
may
forward
speed
clinical
use
induction
treatment.
Advanced Materials,
Journal Year:
2019,
Volume and Issue:
31(51)
Published: Oct. 8, 2019
Abstract
Ferroptosis
is
a
newly
discovered
form
of
regulated
cell
death
that
the
nexus
between
metabolism,
redox
biology,
and
human
health.
Emerging
evidence
shows
potential
triggering
ferroptosis
for
cancer
therapy,
particularly
eradicating
aggressive
malignancies
are
resistant
to
traditional
therapies.
Recently,
there
has
been
great
deal
effort
design
develop
anticancer
drugs
based
on
induction.
Recent
advances
ferroptosis‐inducing
agents
at
intersection
chemistry,
materials
science,
biology
presented.
The
basis
summarized
first
highlight
feasibility
characteristics
therapy.
A
literature
review
inducers
(including
small
molecules
nanomaterials)
then
presented
delineate
their
design,
action
mechanisms,
applications.
Finally,
some
considerations
research
spotlighted,
followed
by
discussion
challenges
future
development
directions
this
burgeoning
field.
Journal of Hematology & Oncology,
Journal Year:
2020,
Volume and Issue:
13(1)
Published: Aug. 10, 2020
Abstract
In
recent
years,
cancer
immunotherapy
based
on
immune
checkpoint
inhibitors
(ICIs)
has
achieved
considerable
success
in
the
clinic.
However,
ICIs
are
significantly
limited
by
fact
that
only
one
third
of
patients
with
most
types
respond
to
these
agents.
The
induction
cell
death
mechanisms
other
than
apoptosis
gradually
emerged
as
a
new
treatment
strategy
because
tumors
harbor
innate
resistance
apoptosis.
date,
possibility
combining
two
modalities
not
been
discussed
systematically.
Recently,
few
studies
revealed
crosstalk
between
distinct
and
antitumor
immunity.
pyroptosis,
ferroptosis,
necroptosis
combined
showed
synergistically
enhanced
activity,
even
ICI-resistant
tumors.
Immunotherapy-activated
CD8+
T
cells
traditionally
believed
induce
tumor
via
following
main
pathways:
(i)
perforin-granzyme
(ii)
Fas-FasL.
identified
mechanism
which
suppress
growth
inducing
ferroptosis
provoked
review
relationship
system
activation.
Hence,
this
review,
we
summarize
knowledge
reciprocal
interaction
immunity
mechanisms,
particularly
necroptosis,
three
potentially
novel
immunogenic
death.
Because
evidence
is
derived
from
using
animal
models,
also
reviewed
related
bioinformatics
data
available
for
human
tissues
public
databases,
partially
confirmed
presence
interactions
activation
Molecular Cancer,
Journal Year:
2020,
Volume and Issue:
19(1)
Published: Feb. 27, 2020
Ferroptosis
is
a
novel
mode
of
non-apoptotic
cell
death
induced
by
build-up
toxic
lipid
peroxides
(lipid-ROS)
in
an
iron
dependent
manner.
Cancer-associated
fibroblasts
(CAFs)
support
tumor
progression
and
drug
resistance
secreting
various
bioactive
substances,
including
exosomes.
Yet,
the
role
CAFs
regulating
metabolism
as
well
ferroptosis
cancer
cells
still
unexplored
remains
enigmatic.Ferroptosis-related
genes
gastric
(GC)
were
screened
using
mass
spectrum;
exosomes
isolated
ultra-centrifugation
CAF
secreted
miRNAs
determined
RT-qPCR.
Erastin
was
used
to
induce
ferroptosis,
levels
evaluated
measuring
lipid-ROS,
viability
mitochondrial
membrane
potential.Here,
we
provide
clinical
evidence
show
that
arachidonate
lipoxygenase
15
(ALOX15)
closely
related
with
lipid-ROS
production
cancer,
exosome-miR-522
serves
potential
inhibitor
ALOX15.
By
primary
stromal
cells,
prove
mainly
derived
from
microenvironment.
Moreover,
heterogeneous
nuclear
ribonucleoprotein
A1
(hnRNPA1)
found
mediate
miR-522
packing
into
exosomes,
ubiquitin-specific
protease
7
(USP7)
stabilizes
hnRNPA1
through
de-ubiquitination.
Importantly,
cisplatin
paclitaxel
promote
secretion
activating
USP7/hnRNPA1
axis,
leading
ALOX15
suppression
decreased
accumulation
ultimately
result
chemo-sensitivity.The
present
study
demonstrates
secrete
exosomal
inhibit
targeting
blocking
accumulation.
The
intercellular
pathway,
comprising
USP7,
hnRNPA1,
exo-miR-522
ALOX15,
reveals
new
mechanism
acquired
chemo-resistance
GC.
Signal Transduction and Targeted Therapy,
Journal Year:
2022,
Volume and Issue:
7(1)
Published: June 20, 2022
Abstract
In
recent
years,
immunotherapy
represented
by
immune
checkpoint
inhibitors
(ICIs)
has
led
to
unprecedented
breakthroughs
in
cancer
treatment.
However,
the
fact
that
many
tumors
respond
poorly
or
even
not
ICIs,
partly
caused
absence
of
tumor-infiltrating
lymphocytes
(TILs),
significantly
limits
application
ICIs.
Converting
these
“cold”
into
“hot”
may
ICIs
is
an
unsolved
question
immunotherapy.
Since
it
a
general
characteristic
cancers
resist
apoptosis,
induction
non-apoptotic
regulated
cell
death
(RCD)
emerging
as
new
treatment
strategy.
Recently,
several
studies
have
revealed
interaction
between
RCD
and
antitumor
immunity.
Specifically,
autophagy,
ferroptosis,
pyroptosis,
necroptosis
exhibit
synergistic
responses
while
possibly
exerting
inhibitory
effects
on
responses.
Thus,
targeted
therapies
(inducers
inhibitors)
against
combination
with
exert
potent
activity,
resistant
This
review
summarizes
multilevel
relationship
immunity
RCD,
including
necroptosis,
potential
targeting
improve
efficacy
malignancy.