Frontiers in Oncology,
Год журнала:
2024,
Номер
14
Опубликована: Дек. 20, 2024
Breast
cancer
is
one
of
the
most
prevalent
malignancies
affecting
women
worldwide,
with
its
incidence
increasingly
observed
in
younger
populations.
In
recent
years,
drug
resistance
has
emerged
as
a
significant
challenge
treatment
breast
cancer,
making
it
central
focus
contemporary
research
aimed
at
identifying
strategies
to
overcome
this
issue.
Growing
evidence
indicates
that
inducing
ferroptosis
through
various
mechanisms,
particularly
by
inhibiting
System
Xc
Seminars in Cancer Biology,
Год журнала:
2024,
Номер
unknown
Опубликована: Дек. 1, 2024
Elevated
lipid
metabolism
is
one
of
hallmarks
malignant
tumors.
Lipids
not
only
serve
as
essential
structural
components
biological
membranes
but
also
provide
energy
and
substrates
for
the
proliferation
cancer
cells
tumor
growth.
Cancer
meet
their
needs
by
coordinating
processes
absorption,
synthesis,
transport,
storage,
catabolism.
As
research
in
this
area
continues
to
deepen,
numerous
new
discoveries
have
emerged,
making
it
crucial
scientists
stay
informed
about
developments
metabolism.
In
review,
we
first
discuss
relevant
concepts
theories
or
assumptions
that
help
us
understand
-based
therapies.
We
then
systematically
summarize
latest
advancements
including
mechanisms,
novel
targets,
up-to-date
pre-clinical
clinical
investigations
anti-cancer
treatment
with
targeted
drugs.
Finally,
emphasize
emerging
directions
therapeutic
strategies,
future
prospective
challenges.
This
review
aims
insights
guidance
field
Breast Cancer Basic and Clinical Research,
Год журнала:
2025,
Номер
19
Опубликована: Янв. 1, 2025
Background:
Ferroptosis
is
a
recently
studied
form
of
programmed
cell
death
characterized
by
lipid
peroxides
accumulation
in
the
cells.
This
process
occurs
when
cell’s
antioxidant
capacity
disturbed
resulting
inability
to
detoxify
toxic
peroxides.
Two
major
components
that
regulate
ferroptosis
are
cysteine
and
iron.
Objective:
study
aimed
determine
effect
deficiency
iron
chelation
on
triple-negative
breast
cancer
(TNBC)
lipid-enriched
microenvironment.
Design:
The
has
laboratory-based
experimental
design.
used
MDA-MB-231
line
various
vitro
culture
systems
investigate
research
question.
Methods:
For
first
part
study,
we
subjected
cells
grow
cysteine-absent
adipocyte-conditioned
media.
In
second
half,
treated
with
chelator,
deferoxamine.
BODIPY
imaging
western
blot
were
carried
out
observe
under
2
conditions.
Results:
results
showed
absence
conditioned
media
was
able
reduce
formation
droplets,
which
increased
greater
access
free
fatty
acids
undergo
oxidation,
therefore
inducing
ferroptosis.
On
contrary,
deferoxamine
along
erastin
(ferroptosis-inducing
drug),
an
increase
content
observed,
later
Conclusion:
Our
show
alternative
function
deferoxamine,
one
regulating
droplets
other
ferroptosis,
although
inhibitor
same,
respectively.
Frontiers in Immunology,
Год журнала:
2025,
Номер
16
Опубликована: Янв. 23, 2025
Ferroptosis
is
a
novel
form
of
cell
death
distinct
from
traditional
mechanisms,
characterized
by
the
accumulation
iron
ions
and
production
lipid
peroxides.
It
not
only
affects
survival
tumor
cells
but
also
closely
linked
to
changes
in
microenvironment.
Lung
cancer
one
leading
malignancies
worldwide
terms
incidence
mortality,
its
complex
biological
mechanisms
resistance
make
treatment
challenging.
Recent
studies
have
shown
that
ferroptosis
plays
key
role
onset
progression
lung
cancer,
with
intricate
regulatory
influencing
development
response
therapy.
As
research
into
deepens,
related
molecular
pathways,
such
as
glutamate
metabolism,
antioxidant
defense,
been
gradually
revealed.
However,
clinical
practice,
ferroptosis-based
therapeutic
strategies
for
are
still
their
early
stages.
Challenges
remain,
including
incomplete
understanding
specific
ferroptosis,
insufficient
on
factors,
limited
insight
interactions
within
Therefore,
effective
modulation
enhance
remains
an
urgent
issue.
This
review
summarizes
analyzes
factors
interaction
microenvironment,
further
explores
potential
targeting
ferroptosis.
By
synthesizing
latest
research,
this
paper
aims
provide
new
perspectives
directions
treatment,
goal
advancing
applications.
Interactive Journal of Medical Research,
Год журнала:
2025,
Номер
14, С. e66286 - e66286
Опубликована: Фев. 26, 2025
Background
Ferroptosis,
as
a
novel
modality
of
cell
death,
holds
significant
potential
in
elucidating
the
pathogenesis
and
advancing
therapeutic
strategies
for
breast
cancer.
Objective
This
study
aims
to
comprehensively
analyze
current
ferroptosis
research
future
trends,
guiding
cancer
advancements
innovative
treatment
strategies.
Methods
used
R
package
Bibliometrix
(Department
Economic
Statistical
Sciences
at
University
Naples
Federico
II),
VOSviewer
(Centre
Science
Technology
Studies
Leiden
University),
CiteSpace
(Drexel
University’s
College
Information
Technology),
conduct
bibliometric
analysis
387
papers
on
from
Web
Core
Collection.
The
covers
authors,
institutions,
journals,
countries
or
regions,
publication
volumes,
citations,
keywords.
Results
number
publications
related
this
field
has
surged
annually,
with
China
United
States
collaborating
closely
leading
output.
Sun
Yat-sen
stands
out
among
while
journal
Frontiers
Oncology
author
Efferth
T
contribute
significantly
field.
Highly
cited
within
domain
primarily
focus
induction
ferroptosis,
protein
regulation,
comparisons
other
modes
providing
foundation
treatment.
Keyword
highlights
maturity
glutathione
peroxidase
4-related
research,
subtypes
emerging
motor
themes
tumor
microenvironment,
immunotherapy,
prognostic
models
identified
basic
themes.
Furthermore,
application
nanoparticles
serves
an
additional
complement
Conclusions
status
focuses
exploration
relevant
theoretical
mechanisms,
whereas
trends
mechanisms
emphasize
investigation
strategies,
particularly
clinical
immunotherapy
microenvironment.
Nanotherapy
demonstrated
domain.
Future
directions
should
deepen
accelerate
translation
findings
provide
new
insights
innovation
development
Research Square (Research Square),
Год журнала:
2025,
Номер
unknown
Опубликована: Апрель 21, 2025
Ferroptosis
is
an
iron-dependent
cell
death
pathway
that
involves
multiple
genes
including
the
transferrin
receptor
(TFRC/CD71),
glutathione
peroxidase
4
(GPX4)
and
SLC7A11.
This
study
based
on
hypothesis
orphan
nuclear
4A1
(NR4A1)
NR4A2
maintain
low
levels
of
ferroptosis
in
triple
negative
breast
cancer
(TNBC)
cells
bis-indole
derived
(CDIM)
compounds
act
as
NR4A1/2
ligands
induce
by
enhancing
CD71
expression.
1,1-Bis(3'-indolyl)-1-(3,5-disubstitutedphenyl)methane
(DIM-3,5)
analogs
were
investigated
for
their
cytotoxicity
effects
NR4A1
regulated
induction
cytotoxicity,
western
blot
RT-PCR.
Several
assays
also
determined
enhanced
lipoperoxidation,
reactive
oxygen
species
malondialdehyde
formation
TNBC
cells.
Knockdown
NR4A1,
NR4A2,
Sp1
Sp4
was
carried
out
RNA
interference.
Molecular
mechanisms
NR4A1/2-mediated
regulation
expression
using
CD71-luciferase
promoter
constructs,
overexpression
chromatin
immunoprecipitation
(ChIP)
assays.
Initial
studies
show
DIM-3,5
inverse
NR4A1/NR4A2
agonist
downregulated
pro-oncogenic
responses/gene
products
both
receptors
induced
ROS,
lipoperoxide
this
accompanied
indicators
include
decreased
GPX4
SLC7A11
CD71.
Induction
CD71,
important
biomarker
observed
after
treatment
with
analogs,
knockdown
or
demonstrating
coregulated
receptors.
Moreover,
ChIP
analysis
indicated
acted
ligand-dependent
cofactors
Sp1/4-mediated
a
key
NR4A1/2/Sp
gene
can
be
directly
targeted
agonists
to
Frontiers in Oncology,
Год журнала:
2025,
Номер
15
Опубликована: Май 20, 2025
Purpose
Ferroptosis,
an
iron-dependent
form
of
regulated
cell
death
(RCD),
has
been
proven
to
affect
the
response
antineoplastic
therapies.
However,
little
is
known
about
role
ferroptosis
in
chemotherapy
and
immune
checkpoint
inhibitor
(ICI)
therapy
responses,
as
well
molecular
subtype
identification
triple-negative
breast
cancer
(TNBC).
Methods
We
performed
unsupervised
clustering
stratify
patients
with
TNBC
Fudan
University
Shanghai
Cancer
Center
(FUSCC)
cohort
into
distinct
ferroptosis-related
subtypes
according
expression
eight
genes
(FRGs):
EMC2,
FTH1,
HMOX1,
LPCAT3,
NOX4,
SOCS1,
BAP1,
ISCU.
conducted
Gene
Ontology
(GO)
analysis
gene
set
variation
(GSVA)
characterize
phenotype
enriched
pathways
TNBC.
constructed
FerrScore
model
identify
most
promising
candidate
compounds
predict
ICI
benefits
for
Results
identified
two
different
overall
survival
(OS).
Patients
cluster
1
exhibited
better
OS,
which
had
a
“hot”
tumor
abundant
infiltration
higher
checkpoints
compared
2.
screened
everolimus
drug
high
referring
comprehensive
factors
including
CMap
score,
experimental
evidence,
clinical
trial
status.
Further,
we
confirmed
that
was
potentially
powerful
metric
anti-PD-L1,
anti-PD-1,
anti-PD-1
+
CTLA-4
benefits.
Conclusions
Ferroptosis
reprogrammed
microenvironment
(TME)
classified
subgroups
significantly
OS.
screen
TNBC,
prioritized
treatment
strategies.
Penicilazaphilone
C
(PAC)
is
a
novel
azaphilone
isolated
by
our
research
team.
While
known
for
its
antitumor
properties,
the
potential
of
PAC
to
trigger
ferroptosis
in
triple-negative
breast
cancer
(TNBC)
cells
remains
unexplored.
This
study
aims
assess
ferroptotic
induction
capability
and
elucidate
underlying
molecular
mechanisms.
Our
results
showed
that
treatment
with
demonstrated
dose-
time-dependent
inhibition
growth
MDA-MB-231
MDA-MB-436
cells.
Flow
cytometry
analysis
lactate
dehydrogenase
assay
revealed
various
forms
cell
death
induced
both
lines.
Specifically,
flow
analyzed
7-AAD-stained
dead
cells,
markers,
such
as
lipid
peroxidation
BODIPY-C11
Fe2+
ions,
identified
major
type
pathway
PAC.
Moreover,
co-administration
inhibitor
Fer-1
notably
mitigated
PAC-induced
death,
further
highlighting
primary
mechanism
through
which
inhibits
TNBC
proliferation.
Further
exploration
mechanisms
unveiled
modulated
expression
Mouse
double
minute
2
(MDM2),
p53,
SLC7A11,
GPX4.
In
vivo
experiments
using
nude
mouse
models
implanted
effectively
suppressed
tumor
growth,
increased
levels
ions
single
downregulated
MDM2
expression,
upregulated
GPX4
expression.
These
suggest
hinders
proliferation
modulating
MDM2/p53/SLC7A11/GPX4
axis
induce
ferroptosis,
positioning
promising
candidate
therapy.
Journal of Biochemical and Molecular Toxicology,
Год журнала:
2024,
Номер
39(1)
Опубликована: Дек. 18, 2024
ABSTRACT
Lung
adenocarcinoma
(LUAD)
is
a
common
type
of
lung
cancer
with
complicated
pathological
mechanism.
Transcription
Factor
AP‐2
Alpha
(TFAP2A)
and
Cysteine
protease
inhibitor
1
(CST1)
are
upregulated
genes
in
LUAD
samples,
accordingly,
we
focused
on
clarifying
the
role
TFAP2A/CST1
axis
LUAD.
Expression
analysis
was
performed
using
real‐time
quantitative
polymerase
chain
reaction
western
blot.
Cellular
behaviors
were
detected
by
colony
formation
assay,
EdU
wound
healing
assay
flow
cytometry.
Ferroptosis
assessed
oxidative
indicators,
Fe
2+
level
related
proteins.
TFAP2A
CST1
interaction
analyzed
via
ChIP
dual‐luciferase
reporter
assay.
function
vivo
evaluated
xenograft
tumor
overexpressed
samples
cells.
Downregulation
inhibited
proliferation,
migration
but
it
promoted
apoptosis
ferroptosis
interacted
promoter
to
up‐regulate
expression.
regulated
malignant
cells
targeting
CST1.
affected
growth
mediating
All
these
data
proved
that
contributed
while
suppressed