Advanced Science,
Год журнала:
2025,
Номер
unknown
Опубликована: Фев. 14, 2025
Abstract
Designing
drugs
to
intelligently
respond
different
ratio
of
biological
electron
donors/receptors
in
cancer
cells
and
normal
is
a
promising
strategy
achieve
highly
effective
less
toxic
chemotherapy.
Herein
by
employing
metal
center
active
the
selenium‐containing
electrophilic
drug
Ru(phtpy‐NO
2
)(phenSe)Cl
(
RuSe
)
with
strongly
polarization
characteristics
are
synthesized
which
can
efficiently
shuttle
electrons
from
donors
convert
oxidative
stress.
The
rate
transfer
at
selenium
1.81
times
higher
cell
environments
compared
environments.
This
results
being
14.98
more
lethal
than
cells.
Experimental
demonstrate
that
transport
process
carried
out
via
radicals
intermediate
positively
correlated
properties
atoms.
transports
bioactive
generate
large
number
superoxide
anions
leading
DNA
damage
decrease
mitochondrial
membrane
potential
further
activates
p53
signaling
pathway
amplifies
cell‐killing
effect
after
transporting
electrons.
work
provides
new
avenue
for
design
efficient
chemotherapeutic
agents.
Drug Resistance Updates,
Год журнала:
2023,
Номер
72, С. 101018 - 101018
Опубликована: Ноя. 11, 2023
Cuproptosis
is
a
newly
identified
form
of
cell
death
driven
by
copper.
Recently,
the
role
copper
and
triggered
in
pathogenesis
cancers
have
attracted
attentions.
has
garnered
enormous
interest
cancer
research
communities
because
its
great
potential
for
therapy.
Copper-based
treatment
exerts
an
inhibiting
tumor
growth
may
open
door
chemotherapy-insensitive
tumors.
In
this
review,
we
provide
critical
analysis
on
homeostasis
dysregulation
development
progression
cancers.
Then
core
molecular
mechanisms
cuproptosis
discussed,
followed
summarizing
current
understanding
copper-based
agents
(copper
chelators,
ionophores,
complexes-based
dynamic
therapy)
treatment.
Additionally,
summarize
emerging
data
ionophores
to
subdue
chemotherapy
resistance
different
types
We
also
review
small-molecule
compounds
nanoparticles
(NPs)
that
kill
cells
inducing
cuproptosis,
which
will
shed
new
light
anticancer
drugs
through
future.
Finally,
important
concepts
pressing
questions
future
should
be
focused
were
discussed.
This
article
suggests
targeting
could
novel
antitumor
therapy
strategy
overcome
drug
resistance.
Cells,
Год журнала:
2023,
Номер
12(5), С. 804 - 804
Опубликована: Март 4, 2023
Ferroptosis
is
a
form
of
regulated
cell
death
that
intricately
linked
to
cellular
metabolism.
In
the
forefront
research
on
ferroptosis,
peroxidation
polyunsaturated
fatty
acids
has
emerged
as
key
driver
oxidative
damage
membranes
leading
death.
Here,
we
review
involvement
(PUFAs),
monounsaturated
(MUFAs),
lipid
remodeling
enzymes
and
in
highlighting
studies
revealing
how
using
multicellular
model
organism
Caenorhabditis
elegans
contributes
understanding
roles
specific
lipids
mediators
ferroptosis.
Signal Transduction and Targeted Therapy,
Год журнала:
2023,
Номер
8(1)
Опубликована: Дек. 10, 2023
Abstract
Ferroptosis,
a
unique
modality
of
cell
death
with
mechanistic
and
morphological
differences
from
other
modes,
plays
pivotal
role
in
regulating
tumorigenesis
offers
new
opportunity
for
modulating
anticancer
drug
resistance.
Aberrant
epigenetic
modifications
posttranslational
(PTMs)
promote
resistance,
cancer
progression,
metastasis.
Accumulating
studies
indicate
that
can
transcriptionally
translationally
determine
vulnerability
to
ferroptosis
functions
as
driver
nervous
system
diseases
(NSDs),
cardiovascular
(CVDs),
liver
diseases,
lung
kidney
diseases.
In
this
review,
we
first
summarize
the
core
molecular
mechanisms
ferroptosis.
Then,
roles
processes,
including
histone
PTMs,
DNA
methylation,
noncoding
RNA
regulation
such
phosphorylation,
ubiquitination,
SUMOylation,
acetylation,
ADP-ribosylation,
are
concisely
discussed.
The
PTMs
genesis
cancers,
NSD,
CVDs,
well
application
PTM
modulators
therapy
these
then
discussed
detail.
Elucidating
mediated
by
will
facilitate
development
promising
combination
therapeutic
regimens
containing
or
PTM-targeting
agents
inducers
be
used
overcome
chemotherapeutic
resistance
could
prevent
addition,
highlight
potential
approaches
chemoresistance
halt
Biomedicine & Pharmacotherapy,
Год журнала:
2024,
Номер
171, С. 116115 - 116115
Опубликована: Янв. 5, 2024
Ferroptosis
and
cuproptosis,
regulated
forms
of
cell
death
resulting
from
metal
ion
accumulation,
are
closely
related
in
terms
occurrence,
metabolism,
signaling
pathways,
drug
resistance.
Notably,
it
is
now
understood
that
these
processes
play
crucial
roles
regulating
physiological
pathological
processes,
especially
tumor
development.
Consequently,
ferroptosis
cuproptosis
have
gained
increasing
significance
as
potential
targets
for
anti-cancer
This
article
systematically
outlines
the
molecular
mechanisms
cross-talk
components
both
elucidating
their
impacts
on
cancer.
Furthermore,
investigates
clinical
perspective
targeted
cancer
chemotherapy,
immunotherapy,
radiotherapy.
Our
discussion
extends
to
a
comparative
analysis
nanoparticles
developed
based
cancer,
contrasting
them
with
current
conventional
therapies.
Opportunities
challenges
treatment
explored,
emphasizing
therapeutic
direction
co-targeting
cuproptosis.
The
also
attempts
analyze
applications
this
approach
while
summarizing
existing
barriers
require
overcoming.
In
recent
years,
the
incidence
of
gastrointestinal
cancers
is
increasing,
particularly
in
younger
population.
Effective
treatment
crucial
for
improving
patients'
survival
outcomes.
Programmed
cell
death,
regulated
by
various
genes,
plays
a
fundamental
role
growth
and
development
organisms.
It
also
critical
maintaining
tissue
organ
homeostasis
takes
part
multiple
pathological
processes.
addition
to
apoptosis,
there
are
other
types
programmed
such
as
ferroptosis,
necroptosis,
pyroptosis,
which
can
induce
severe
inflammatory
responses.
Notably,
besides
pyroptosis
contribute
occurrence
cancers.
This
review
aims
provide
comprehensive
summary
on
biological
roles
molecular
mechanisms
well
their
regulators
hope
open
up
new
paths
tumor
targeted
therapy
near
future.
Abstract
Ferroptosis
is
a
new
form
of
regulated
cell
death
featuring
iron‐dependent
lipid
peroxides
accumulation
to
kill
tumor
cells.
A
growing
body
evidence
has
shown
the
potential
ferroptosis‐based
cancer
therapy
in
eradicating
refractory
malignancies
that
are
resistant
apoptosis‐based
conventional
therapies.
In
recent
years,
studies
have
reported
number
ferroptosis
inducers
can
increase
vulnerability
cells
by
regulating
ferroptosis‐related
signaling
pathways.
Encouraged
rapid
development
ferroptosis‐driven
therapies,
interdisciplinary
fields
combine
ferroptosis,
pharmaceutical
chemistry,
and
nanotechnology
focused.
First,
prerequisites
metabolic
pathways
for
briefly
introduced.
Then,
detail
emerging
designed
boost
ferroptosis‐induced
therapy,
including
metal
complexes,
metal‐based
nanoparticles,
metal‐free
nanoparticles
summarized.
Subsequently,
application
synergistic
strategies
with
apoptosis
other
emphasis
on
use
both
cuproptosis
induce
redox
dysregulation
intracellular
bimetallic
copper/iron
metabolism
disorders
during
treatment
discussed.
Finally,
challenges
associated
clinical
translation
future
directions
potentiating
therapies
highlighted.
Free Radical Biology and Medicine,
Год журнала:
2024,
Номер
220, С. 125 - 138
Опубликована: Апрель 22, 2024
Fusobacterium
(F.)
nucleatum
is
a
carcinogenesis
microbiota
in
colorectal
cancer
(CRC).
Growing
evidence
shows
that
F.
contributes
to
chemoresistance.
Ferroptosis
reported
restore
the
susceptibility
of
resistant
cells
chemotherapy.
However,
role
gut
affecting
ferroptosis
chemoresistance
remains
unclear.
Here,
we
examined
CRC
tissues
patients
using
16S
rRNA
sequencing
investigate
possible
connection
between
dysbiosis
and
relapse
CRC.
We
found
high
abundance
tissue
associated
with
relapse.
further
demonstrated
induced
oxaliplatin
resistance
vitro
vivo.
The
transcriptome
an
nucleatum-infected
cell
revealed
was
infection.
perform
malondialdehyde,
ferrous
iron,
glutathione
assays
verify
effect
on
under
treatment
vivo
vitro.
Mechanistically,
promoted
by
overexpressing
GPX4
then
inhibiting
ferroptosis.
E-cadherin/β-catenin/TCF4
pathway
conducted
overexpression
nucleatum.
chromatin
immuno-precipitation
quantitative
PCR
(CHIP-qPCR)
dual-luciferase
reporter
assay
showed
TCF4
binding
GPX4.
also
determined
E-cadherin/β-catenin/TCF4/GPX4
axis
related
tumor
status
clinically.
contribution
Targeting
will
provide
valuable
insight
into
management
may
improve
outcomes
for
