Chemical Reviews,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Feb. 14, 2025
Ferroptosis,
an
iron-dependent
form
of
regulatory
cell
death,
has
garnered
significant
interest
as
a
therapeutic
target
in
cancer
treatment
due
to
its
distinct
characteristics,
including
lipid
peroxide
generation
and
redox
imbalance.
However,
clinical
application
oncology
is
currently
limited
by
issues
such
suboptimal
efficacy
potential
off-target
effects.
The
advent
nanotechnology
provided
new
way
for
overcoming
these
challenges
through
the
development
activatable
magnetic
nanoparticles
(MNPs).
These
innovative
MNPs
are
designed
improve
specificity
ferroptosis
induction.
This
Review
delves
into
chemical
biological
principles
guiding
design
ferroptosis-based
therapies
imaging-guided
therapies.
It
discusses
mechanisms
attributes
ferroptosis,
composition
MNPs,
their
mechanism
action
inducers,
integration
with
advanced
imaging
techniques
monitoring.
Additionally,
we
examine
convergence
other
strategies,
chemodynamic
therapy,
photothermal
photodynamic
sonodynamic
immunotherapy,
within
context
nanomedicine
strategies
utilizing
MNPs.
highlights
multifunctional
surpass
limitations
conventional
treatments,
envisioning
future
drug-resistance-free,
precision
diagnostics
treating
recalcitrant
cancers.
Heliyon,
Journal Year:
2024,
Volume and Issue:
10(18), P. e37613 - e37613
Published: Sept. 1, 2024
Oxaliplatin
(OXA)-based
therapy
is
effective
in
the
treatment
of
multiple
cancers.
However,
primary
or
acquired
OXA
resistance
remains
an
emerging
challenge
for
its
clinical
application.
Ferroptosis
iron-dependent
mode
cell
death
that
has
been
demonstrated
to
play
essential
role
chemoresistance
many
drugs,
including
OXA.
In
particular,
dysregulation
SLC7A11-GPX4,
one
major
antioxidant
systems
ferroptosis,
was
found
colorectal
cancer
(CRC)
and
hepatocellular
carcinoma
(HCC).
addition,
Nrf2,
upstream
regulator
GPX4
other
factors,
also
involved
CRC
HCC.
Inhibition
SLC7A11-GPX4
Nrf2
by
genetic
deletion
pharmaceutical
inhibition
could
significantly
reverse
resistance.
Long
noncoding
RNA
(lncRNA)
participates
ferroptosis
cells.
Specifically,
LINC01134
promotes
recruitment
promoter
GPX4,
thereby
exerting
transcriptional
regulation
which
eventually
increases
sensitivity
HCC
through
upregulation
ferroptosis.
On
hand,
a
novel
lncRNA
DACT3-AS1
sensitizes
gastric
cells
miR-181a-5p/sirtuin
1(SIRT1)-mediated
Therapies
based
on
combination
enhancers
provide
new
therapeutic
insights
overcome
present
review,
we
current
understanding
ferroptosis-related
resistance,
highlight
pathogenesis
chemoresistance,
summarize
available
therapies
target
enhancing
Advanced Science,
Journal Year:
2025,
Volume and Issue:
unknown
Published: April 11, 2025
Abstract
Small
cell
lung
cancer
(SCLC)
is
an
extremely
aggressive
and
highly
malignant
type
of
that
frequently
develops
resistance
recurrence
following
initial
treatment.
Paclitaxel
(PTX)
a
second‐line
therapeutic
option
for
SCLC
patients
with
to
first‐line
However,
its
clinical
application
limited
due
suboptimal
efficacy
the
risk
hypersensitivity
reactions.
To
address
these
challenges,
novel
strategy
employing
cationic
liposome‐based
biomimetic
drug
co‐delivery
system,
siPFKFB4/PRL
PTX
@RBCM‐cRGD,
which
simultaneously
delivers
paclitaxel
PFKFB4‐targeting
small
interfering
RNA
(siRNA)
cells
tissues
proposed.
These
findings
demonstrate
this
system
can
induce
ferroptosis
in
cells,
thereby
enhancing
their
sensitivity
paclitaxel.
Moreover,
It
promotes
infiltration
immune
secretion
cytokines
within
microenvironment,
effectively
activating
anti‐tumor
immunity.
When
combined
anti‐PD‐L1
antibodies,
it
further
potentiates
responses.
results
suggest
codelivery
not
only
induces
enhance
but
also
reprograms
potentiating
effects
immunotherapy
providing
promising
new
SCLC.
APOPTOSIS,
Journal Year:
2024,
Volume and Issue:
unknown
Published: June 9, 2024
Abstract
Ferroptosis
is
a
form
of
cell
death
that
triggered
by
the
presence
ferrous
ions
and
characterized
lipid
peroxidation
induced
these
ions.
The
mechanism
exhibits
distinct
morphological
characteristics
compared
to
apoptosis,
autophagy,
necrosis.
A
notable
aspect
ferroptosis
its
ability
inhibit
uncontrolled
tumor
replication
immortalization,
especially
in
malignant,
drug-resistant,
metastatic
tumors.
Additionally,
immunotherapy,
novel
therapeutic
approach
for
tumors,
has
been
found
have
reciprocal
regulatory
relationship
with
context
anti-tumor
therapy.
comprehensive
analysis
immunotherapy
therapy
presented
this
paper,
highlighting
potential
mutual
adjuvant
effects.
Specifically,
we
discuss
mechanisms
underlying
emphasizing
their
improve
immune
microenvironment
enhance
immunotherapeutic
Furthermore,
investigate
how
factors
may
increase
sensitivity
cells
ferroptosis.
We
aim
provide
prospective
view
promising
value
combined
anticancer
elucidating
network
between
each.
Graphical
involves
intricate
crosstalk
cells.
Through
MHC
recognition,
CD8
+
T
activate
JAK1/STAT1
pathway
cells,
impairing
function
System
Xc
reducing
GSH
GPX4
expression
promote
activation
STAT1-IRF1-ACSL4
could
also
blockade
antioxidant
induces
ferroptosis,
released
DAMPs
DCs
maturation
through
cGAMP-STING-TBK1
pathway,
leading
antigen
presentation
activates
release
M1-type
polarization
macrophages,
which
exerts
an
effect.
effects
be
enhanced
blocking
inhibitory
checkpoints
such
as
PD-1,
PD-L1,
CTLA4,
LAG3.
Abbreviations:
ACSL4,
acyl-CoA
synthetase
long-chain
family
member
4;
BH4,
tetrahydrobiopterin;
cGAMP,
cyclic
GMP-AMP;
cytotoxic
lymphocyte-associated
antigen-4;
DCs,
dendritic
cells;
DHFR,
dihydrofolate
reductase;
DHODH,
dihydroorotate
dehydrogenase;
GPX4,
glutathione
peroxidase
GSH,
glutathione;
HIF-1α,
Hypoxia-Inducible
Factor-1α;IFN-γ,
interferon-γ;
IRF1,
interferon
factor
1;IRP1,
iron
protein
1;
JAK
1,
janus
kinase;
LAG3,
lymphocyte
gene
3;
MHC,
major
histocompatibility
complex;
NRF2,
nuclear
erythroid-2-related
2;
programmed
-1;
ligand
PUFA,
polyunsaturated
fatty
acid;
ROS,
reative
oxygen
species;
STAT1,
signal
transducer
activator
transcription
STING,
stimulator
genes;
TBK1,
TANK-binding
kinase
1
TLR2,
toll-like
receptor
2.
This
diagram
was
drawn
Figdraw
(
www.figdraw.com
).
