Journal of Materials Chemistry B,
Год журнала:
2024,
Номер
unknown
Опубликована: Янв. 1, 2024
Cuproptosis
is
a
regulated
form
of
cell
death
induced
by
the
accumulation
metal
ions
and
closely
linked
to
aspects
cellular
drug
resistance,
metabolism,
signalling
pathways.
Due
its
crucial
role
in
regulating
physiological
pathological
processes,
cuproptosis
has
gained
increasing
significance
as
potential
target
for
anticancer
development.
In
this
review,
we
introduce
definition
provide
comprehensive
discussion
mechanisms
cuproptosis.
addition,
methods
detection
are
summarized,
recent
advances
cancer
therapy
reviewed,
mainly
terms
elesclomol
(ES)-mediated
disulfiram
(DSF)-mediated
cuproptosis,
which
provided
practical
value
applications.
Finally,
current
challenges
future
development
cuproptosis-mediated
discussed.
summary,
review
highlights
progress
on
therapy,
offering
novel
ideas
strategies
research
Abstract
The
induction
of
cuproptosis,
a
recently
identified
form
copper‐dependent
immunogenic
cell
death,
is
promising
approach
for
antitumor
therapy.
However,
sufficient
accumulation
intracellular
copper
ions
(Cu
2+
)
in
tumor
cells
essential
inducing
cuproptosis.
Herein,
an
intelligent
cuproptosis‐inducing
nanosystem
constructed
by
encapsulating
oxide
(CuO)
nanoparticles
with
the
ionophore
elesclomol
(ES).
After
uptake
cells,
ES@CuO
degraded
to
release
Cu
and
ES
synergistically
trigger
thereby
significantly
inhibiting
growth
murine
B16
melanoma
cells.
Moreover,
further
promoted
cuproptosis‐mediated
immune
responses
reprogrammed
immunosuppressive
microenvironment
increasing
number
tumor‐infiltrating
lymphocytes
secreted
inflammatory
cytokines.
Additionally,
combining
programmed
death‐1
(PD‐1)
immunotherapy
substantially
increased
efficacy
melanoma.
Overall,
findings
this
study
can
lead
use
novel
strategy
therapy,
which
may
enhance
checkpoint
inhibitor
Despite
the
initial
efficacy
of
enzalutamide
in
castration-resistant
prostate
cancer
(CRPC),
inevitable
resistance
remains
a
significant
challenge.
Here,
synergistic
induction
copper-dependent
cell
death
(cuproptosis)
CRPC
cells
is
reported
by
and
copper
ionophores
(elesclomol/disulfiram).
Mechanistically,
treatment
increases
mitochondrial
dependence
cells,
rendering
them
susceptible
to
cuproptosis,
as
evidenced
specific
reversal
with
chelator
tetrathiomolybdate.
This
susceptibility
characterized
hallmarks
including
lipoylated
protein
aggregation
iron-sulfur
cluster
instability.
Interestingly,
matrix
reductase,
FDX1,
specifically
correlates
elesclomol
sensitivity,
suggesting
potential
mechanistic
divergence
between
two
ionophores.
Notably,
this
effect
extends
beyond
vitro
models,
demonstrating
22Rv1
xenografts,
mouse
Pten
p53
knockout
organoids.
Importantly,
significantly
enhances
ionophore-mediated
cytotoxicity
enzalutamide-resistant
cells.
Collectively,
these
findings
indicate
that
synergistically
induce
offering
promising
therapeutic
avenue
for
CRPC,
potentially
cases.
Objectives:
To
advance
our
knowledge
of
disease
mechanisms
and
therapeutic
options,
understanding
cell
cycle
regulation
is
critical.
Recent
research
has
highlighted
the
importance
reactive
oxygen
species
(ROS)
in
regulation.
Although
excessive
ROS
levels
can
lead
to
age-related
pathologies,
also
play
an
essential
role
normal
cellular
functions.
Many
regulatory
proteins
are
affected
by
their
redox
status,
but
precise
conditions
under
which
promote
or
inhibit
proliferation
not
fully
understood.
Cell Death and Disease,
Год журнала:
2024,
Номер
15(11)
Опубликована: Ноя. 20, 2024
Abstract
Copper
(Cu),
an
indispensable
micronutrient
for
the
sustenance
of
living
organisms,
contributes
significantly
to
a
vast
array
fundamental
metabolic
processes.
The
human
body
maintains
relatively
low
concentration
copper,
which
is
mostly
found
in
bones,
liver,
and
brain.
Despite
its
concentration,
Cu
plays
crucial
role
as
element
progression
pathogenesis
central
nervous
system
(CNS)
diseases.
Extensive
studies
have
been
conducted
recent
years
on
copper
homeostasis
copper-induced
cell
death
CNS
disorders,
including
glioma,
Alzheimer’s
disease,
Amyotrophic
lateral
sclerosis,
Huntington’s
stroke.
Cuproptosis,
novel
pathway
distinct
from
apoptosis,
necrosis,
pyroptosis,
ferroptosis,
has
identified
potentially
intricately
linked
pathogenic
mechanisms
underlying
various
Therefore,
systematic
review
cuproptosis
their
relationship
with
disorders
could
deepen
our
understanding
these
In
addition,
it
may
provide
new
insights
strategies
treatment
disorders.
Biomedicine & Pharmacotherapy,
Год журнала:
2024,
Номер
176, С. 116874 - 116874
Опубликована: Июнь 7, 2024
Copper,
an
indispensable
micronutrient,
is
implicated
in
numerous
vital
biological
processes
and
essential
for
all
physiological
activities.
Recently,
the
discovery
of
a
novel
type
copper-dependent
cell
death,
known
as
cuproptosis,
has
shed
light
on
its
role
cancer
development.
Extensive
research
currently
underway
to
unravel
mechanisms
underlying
cuproptosis
correlation
with
various
types.
In
this
review,
we
summarize
findings
regarding
roles
types,
including
colorectal
cancer,
lung
gastric
breast
liver
cutaneous
melanoma.
Furthermore,
effects
copper-related
agents
such
copper
chelators
ionophores
proliferation,
apoptosis,
angiogenesis,
tumor
immunity,
chemotherapy
resistance
have
been
explored
preclinical
clinical
trials.
These
insights
provide
promising
avenues
development
prospective
anticancer
drugs
aimed
at
inducing
cuproptosis.
Advanced Science,
Год журнала:
2025,
Номер
unknown
Опубликована: Март 24, 2025
Studies
show
that
intracellular
accumulation
of
copper
ions
causes
cuproptosis,
potentially
enhancing
anticancer
immunity.
However,
the
induction
cuproptosis
inevitably
faces
challenges
due
to
low
deliver
efficiency
and
collateral
damage
normal
tissues.
This
paper
presents
a
self-amplified
nanoplatform
(CEL
NP)
composed
Cu2-
XS
hollow
nanospheres
(HNSs),
elesclomol
(ES),
phase-change
material
lauric
acid
(LA).
Under
NIR-II
laser
irradiation,
photothermal
energy
generated
by
HNSs
melts
LA,
facilitating
precise
release
ES
within
tumor
microenvironment.
Notably,
can
traverse
cell
membrane
form
ES-Cu(II)
complexes,
thereby
delivery
cells.
Excess
Cu(II)
also
reacts
with
endogenous
glutathione,
reducing
its
inhibitory
effect
on
cuproptosis.
Ultimately,
this
amplified
activate
immunogenic
death,
eliciting
robust
immune
response
promoting
suppression.
The
CEL
NP-mediated
offers
novel
approach
for
therapy
through
induction.
Cancer Drug Resistance,
Год журнала:
2025,
Номер
unknown
Опубликована: Март 26, 2025
Cancer
cells
often
develop
tolerance
to
chemotherapy,
targeted
therapy,
and
immunotherapy
drugs
either
before
or
during
treatment.
The
significant
heterogeneity
among
various
tumors
poses
a
critical
challenge
in
modern
cancer
research,
particularly
overcoming
drug
resistance.
Copper,
as
an
essential
trace
element
the
body,
participates
biological
processes
of
diseases,
including
cancers.
growth
many
types
tumor
exhibits
heightened
dependence
on
copper.
Thus,
targeting
copper
metabolism
inducing
cuproptosis
may
be
potential
ways
overcome
Copper
chelators
have
shown
resistance
by
copper-dependent
cells.
In
contrast,
ionophores,
copper-based
nanomaterials,
other
small
molecules
been
used
induce
cell
death
(cuproptosis)
cells,
drug-resistant
This
review
summarizes
regulation
role
resistance,
providing
ideas
for
future.
