Abstract
Nanomedicine‐assisted
sonodynamic
therapy
(SDT)
has
emerged
as
one
of
the
most
promising
cancer
therapies
due
to
its
unique
advantages
high
penetration,
non‐radiation,
and
excellent
oxidative
stress
effect,
but
always
suffered
from
self‐protection
mechanism
apoptosis
resistance
characteristics
evolutionarily
mutated
cells.
Regulated
cell
death
(RCD)
received
increasing
attention
in
precision
treatments
because
significant
role
synergistically
sensitizing
reversing
immunosuppressive
microenvironment
during
SDT
nanomedicine‐triggered
immunogenic
death.
Herein,
paradigmatic
research
RCD‐augmented
tumor
immunotherapeutics
are
typically
introduced,
such
autophagy
blockade,
ferroptosis
targeting,
pyroptosis
induction,
necroptosis
initiation,
cuproptosis
actuation,
PANoptosis
trigger,
coordinated
anti‐tumor
mechanisms
discussed
detail.
Multiple
analysis
focusing
on
currently
unsolved
problems
future
development
prospects
RCD‐based
nano‐oncology
medicine
also
prospected
further
strengthen
expand
scope
therapeutic
applications.
Cancer Cell International,
Год журнала:
2024,
Номер
24(1)
Опубликована: Фев. 9, 2024
Abstract
The
incidence
of
melanoma,
the
most
lethal
form
skin
cancer,
has
increased
due
to
ultraviolet
exposure.
treatment
advanced
particularly
metastatic
cases,
remains
challenging
with
poor
outcomes.
Targeted
therapies
involving
BRAF/MEK
inhibitors
and
immunotherapy
based
on
anti-PD1/anti-CTLA4
antibodies
have
achieved
long-term
survival
rates
approximately
50%
for
patients
melanoma.
However,
therapy
resistance
inadequate
response
continue
hinder
further
breakthroughs
in
treatments
that
increase
rates.
This
review
provides
an
introduction
molecular-level
pathogenesis
melanoma
offers
overview
current
options
their
limitations.
Cells
can
die
by
either
accidental
or
regulated
cell
death
(RCD).
RCD
is
orderly
controlled
a
variety
macromolecules
maintain
stability
internal
environment.
Since
uncontrolled
proliferation
tumor
cells
requires
evasion
programs,
inducing
may
be
strategy.
summarizes
studies
various
types
nonapoptotic
RCDs,
such
as
autophagy-dependent
death,
necroptosis,
ferroptosis,
pyroptosis,
recently
discovered
cuproptosis,
context
relationships
between
these
RCDs
are
examined,
interplay
targeted
discussed.
Given
findings
demonstrating
different
stimuli
associated
induction
shows
promise
integral
component
strategies
Molecular Carcinogenesis,
Год журнала:
2025,
Номер
unknown
Опубликована: Фев. 23, 2025
ABSTRACT
Cuproptosis
is
a
form
of
programmed
cell
death
dependent
on
mitochondrial
respiration
and
crucial
in
cancer
treatment.
The
study
attempted
to
screen
cuproptosis‐associated
genes
colorectal
(CRC)
reveal
regulatory
pathways.
Weighted
gene
co‐expression
network
analysis
(WGCNA)
was
applied
the
modules
based
expression
CRC
patients.
were
screened
at
intersection
cuproptosis
data
set.
RNA
sequencing
performed
assess
transcriptome
changes,
followed
by
functional
enrichment
analyses
potential
Ferredoxin
1
(FDX1)
knocked
down
vivo
vitro
experiments
investigate
effects
FDX1
knockdown
progression
cuproptosis.
found
as
highly
expressed
tumor
cells.
Knockdown
regulated
cells,
inhibited
growth,
migration
invasion.
We
1956
upregulated
DEGs
2201
downregulated
si‐FDX1
which
mainly
enriched
mitogen‐activated
protein
kinase
(MAPK)
signaling
pathway,
necrosis
factor
(TNF)
pathway
Hippo
pathway.
increasing
levels
dihydrolipoamide
S‐succinyltransferase
(DLST),
lipoic
acid
synthetase
(LIAS)
phosphorylation
Yes‐associated
(pYAP)/YAP,
transcriptional
coactivator
with
PDZ‐binding
domain
(TAZ).
inhibitor
GA‐017
blocked
this
process.
Knocking
mediating
shed
new
insights
into
development
biomarkers
for
ACS Applied Materials & Interfaces,
Год журнала:
2025,
Номер
unknown
Опубликована: Март 19, 2025
The
application
of
2D
nanomaterials
for
drug
delivery
via
π-π
interactions
has
been
extensively
investigated.
However,
these
often
lack
robustness
in
the
presence
blood
proteins
due
to
competitive
binding
proteins,
which
results
from
strong
π-π-stacking
with
aromatic
protein
residues.
This
can
lead
premature
release
and
diminished
therapeutic
efficacy.
To
address
this
challenge,
we
developed
a
robust
delivery/therapeutic
biomimetic
nanoplatform
that
enhances
adsorption
affinity
targeted
efficiency
chemotherapeutic
doxorubicin
(DOX)
by
utilizing
Cu2+-modified
black
phosphorus
nanosheets
(BP@Cu2+)
through
metal
ion-assisted
interactions.
synergistic
between
π-electrons
BP
DOX,
mediated
Cu2+
coordination,
form
stable
sandwiched
π-cation-π
stacking
complex
(BP@Cu2+/DOX).
metal-ion-bridged
architecture
significantly
DOX
loading
capacity
minimizes
serum.
In
acidic
tumor
microenvironment,
interaction
is
disrupted,
enabling
controlled
both
ions.
Furthermore,
encapsulation
within
cell
membranes
targeting,
resulting
(BP@Cu2+/DOX-CMs).
Combined
near-infrared
laser
irradiation,
achieves
multimodal
therapy
integrating
phototherapy,
chemotherapy,
chemodynamic
therapy,
cuproptosis
enhance
antitumor
study
highlights
potential
development
advanced
nanoplatforms,
thereby
paving
way
innovative
biomedical
applications
conventional
nanomaterials.
Advanced Biology,
Год журнала:
2025,
Номер
unknown
Опубликована: Апрель 9, 2025
Abstract
Ferroptosis,
as
novel
type
of
regulated
cell
death
that
has
garnered
widespread
attention
over
the
past
decade,
witnessed
continuous
discovery
an
increasing
number
regulatory
mechanisms.
Trace
metal
elements
play
a
multifaceted
and
crucial
role
in
oncology.
Interestingly,
it
been
increasingly
evident
these
elements,
such
copper,
are
involved
regulation
iron
accumulation,
lipid
peroxidation
antiferroptotic
systems,
suggesting
existence
“nonferrous”
mechanisms
ferroptosis.
In
this
review,
comprehensive
overview
composition
mechanism
ferroptosis
is
provided.
The
interaction
between
copper
metabolism
(including
cuproptosis)
cancer,
well
roles
other
trace
(such
zinc,
manganese,
cobalt,
molybdenum)
specifically
focused.
Furthermore,
applications
nanomaterials
based
on
metals
cancer
therapy
also
reviewed
potential
strategies
for
co‐targeting
cuproptosis
explored.
Nevertheless,
light
intricate
ambiguous
nature
interactions,
ongoing
research
essential
to
further
elucidate
ferroptosis,
thereby
facilitating
development
therapeutic
targets
approaches
treatment.
Copper
is
a
vital
trace
element
in
human
physiology,
essential
for
the
synthesis
of
numerous
crucial
metabolic
enzymes
and
facilitation
various
biological
processes.
Regulation
copper
levels
within
narrow
range
imperative
maintaining
homeostasis.
Numerous
studies
have
demonstrated
significant
roles
homeostasis
cuproptosis
health
disease
pathogenesis.
However,
comprehensive
up-to-date
systematic
review
this
domain
remains
absent.
This
aims
to
consolidate
recent
advancements
understanding
disease,
focusing
on
underlying
mechanisms
potential
therapeutic
interventions.
Dysregulation
homeostasis,
manifesting
as
either
excess
or
deficiency,
implicated
etiology
diseases.
Cuproptosis,
recently
identified
form
cell
death,
characterized
by
intracellular
overload.
phenomenon
mediates
diverse
array
evolutionary
processes
organisms,
spanning
from
genetic
disorders,
liver
diseases,
neurodegenerative
cancers.
provides
summary
pathogenic
along
with
associated
targeted
agents.
Furthermore,
it
explores
future
research
directions
yield
treatment,
management,
prevention.
Biomarker Research,
Год журнала:
2024,
Номер
12(1)
Опубликована: Окт. 31, 2024
Copper
is
an
important
trace
element
for
maintaining
key
biological
functions
such
as
cellular
respiration,
nerve
conduction,
and
antioxidant
defense.
Maintaining
copper
homeostasis
critical
human
health,
its
imbalance
has
been
linked
to
various
diseases,
especially
cancer.
Cuproptosis,
a
novel
mechanism
of
copper-induced
cell
death,
provides
new
therapeutic
opportunities
metal
ion
regulation
interact
with
fate.
This
review
insights
into
the
complex
mechanisms
metabolism,
molecular
basis
cuproptosis,
association
cancer
development.
We
assess
role
cuproptosis-related
genes
(CRGs)
associated
tumorigenesis,
their
importance
prognostic
indicators
targets,
impact
on
tumor
microenvironment
(TME)
immune
response.
Ultimately,
this
highlights
interplay
between
copper,
immunotherapy.
