International Journal of Nanomedicine,
Journal Year:
2025,
Volume and Issue:
Volume 20, P. 2623 - 2643
Published: March 1, 2025
In
recent
years,
nanobiotechnology,
widely
used
in
hepatoma,
holds
great
promise
for
improving
targeted
hepatocarcinoma
therapy.
On
account
of
the
unique
properties
low
toxicity,
good
tolerance,
biocompatibility,
and
biodegradability
new
nanomaterials,
a
drug
delivery
system
(TDDS)
has
been
constructed,
which
can
boost
therapeutic
effect
hepatoma-targeted
drugs,
reduce
minimize
off
target
reactions
by
enhancing
permeability
retention
(EPR)
active
targeting,
thus
existing
liver
cancer
therapy
strategies.
Different
nanoparticles
have
their
own
advantages
disadvantages.
They
be
loaded
with
multiple
drugs
on
same
nanoparticle
also
surface
modified
each
other
to
achieve
synergistic
anti-tumor
effects.
This
essay
provides
comprehensive
overview
current
status
hepatocarcinoma,
nanoparticles'
structure,
disadvantages
nanoparticle,
application
progress
cancer.
We
hope
provide
basis
future
clinical
hepatoma
using
nanotechnology.
Organic Letters,
Journal Year:
2024,
Volume and Issue:
26(27), P. 5695 - 5699
Published: June 24, 2024
One
rare
stephacidin-asperochratide
hybrid,
stephaochratidin
A
(1),
was
isolated
from
the
deep-sea-derived
Aspergillus
ochraceus
MCCC
3A00521.
The
relative
structure
of
1
determined
by
comprehensive
analyses
its
1D
and
2D
NMR
data
as
well
HRESIMS
data.
And
absolute
configuration
unambiguously
assigned
ECD
calculations
X-ray
single-crystal
diffraction
analysis.
Plausible
biosynthetic
pathway
proposed.
Stephaochratidin
(1)
exhibited
significant
ferroptosis
inhibitory
activity
with
EC50
value
15.4
μM
downregulating
HMOX-1
expression
lipid
peroxidation.
Signal Transduction and Targeted Therapy,
Journal Year:
2024,
Volume and Issue:
9(1)
Published: Dec. 4, 2024
Abstract
The
dynamic
regulation
of
chromatin
accessibility
is
one
the
prominent
characteristics
eukaryotic
genome.
inaccessible
regions
are
mainly
located
in
heterochromatin,
which
multilevel
compressed
and
access
restricted.
remaining
accessible
loci
generally
euchromatin,
have
less
nucleosome
occupancy
higher
regulatory
activity.
opening
most
important
prerequisite
for
DNA
transcription,
replication,
damage
repair,
regulated
by
genetic,
epigenetic,
environmental,
other
factors,
playing
a
vital
role
multiple
biological
progresses.
Currently,
based
on
susceptibility
difference
occupied
or
free
to
enzymatic
cleavage,
solubility,
methylation,
transposition,
there
many
methods
detect
both
bulk
single-cell
level.
Through
combining
with
high-throughput
sequencing,
genome-wide
landscape
tissues
cells
types
also
been
constructed.
feature
distinct
different
states.
Research
network
crucial
uncovering
secret
various
processes.
In
this
review,
we
comprehensively
introduced
major
functions
mechanisms
variation
physiological
pathological
processes,
meanwhile,
targeted
therapies
dynamics
summarized.
Aging,
Journal Year:
2023,
Volume and Issue:
15(22), P. 12952 - 12965
Published: Nov. 16, 2023
Colorectal
cancer
is
one
of
the
most
common
malignant
tumors
in
digestive
system,
and
its
high
incidence
metastasis
rate
make
it
a
terrible
killer
that
threatens
human
health.
In-depth
exploration
targets
affecting
progression
colorectal
cells
development
specific
targeted
drugs
for
them
are
great
significance
prognosis
patients.
Erythropoietin-producing
hepatocellular
A2
(EphA2)
member
Eph
subfamily
with
tyrosine
kinase
activity,
plays
key
role
regulation
signaling
pathways
related
to
phenotype
various
tumor
cells,
but
regulatory
mechanism
needs
be
further
clarified.
Here,
we
found
EphA2
was
abnormally
highly
expressed
patients
expression
had
worse
prognosis.
We
also
can
form
liquid-liquid
phase
separation
condensates
on
cell
membrane,
which
disrupted
by
ALW-II-41-27,
an
inhibitor
EphA2.
In
addition,
positively
correlated
ferroptosis-related
genes
infiltration
multiple
immune
cells.
These
findings
suggest
novel
membrane
protein
ability
associated
ferroptosis
infiltration,
suggests
may
inhibited
suppressing
Frontiers in Pharmacology,
Journal Year:
2024,
Volume and Issue:
15
Published: April 22, 2024
Ferroptosis
is
caused
by
the
accumulation
of
cellular
reactive
oxygen
species
that
exceed
antioxidant
load
glutathione
(GSH)
and
phospholipid
hydroperoxidases
with
GSH-based
substrates
can
carry
When
capacity
cells
reduced,
lipid
accumulate,
which
cause
oxidative
death.
Ferroptosis,
an
iron-dependent
regulatory
necrosis
pathway,
has
emerged
as
a
new
modality
cell
death
strongly
associated
cancer.
Surgery,
chemotherapy
radiotherapy
are
main
methods
cancer
treatment.
However,
resistance
to
these
mainstream
anticancer
drugs
strong
toxic
side
effects
have
forced
development
alternative
treatments
high
efficiency
low
toxicity.
In
recent
years,
increasing
number
studies
shown
traditional
Chinese
medicines
(TCMs),
especially
herbs
or
herbal
extracts,
inhibit
tumor
growth
metastasis
inducing
ferroptosis,
suggesting
they
could
be
promising
agents
for
This
article
reviews
current
research
progress
on
antitumor
TCMs
through
induction
ferroptosis.
The
aim
was
elucidate
potential
mechanisms
targeting
ferroptosis
in
cancer,
findings
lead
directions
reference
values
developing
better
treatment
strategies.
Proceedings of the National Academy of Sciences,
Journal Year:
2024,
Volume and Issue:
122(1)
Published: Dec. 31, 2024
Ferroptosis,
a
unique
form
of
iron-dependent
cell
death
triggered
by
lipid
peroxidation
accumulation,
holds
great
promise
for
cancer
therapy.
Despite
the
crucial
role
GPX4
in
regulating
ferroptosis,
our
understanding
protein
regulation
remains
limited.
Through
FACS-based
genome-wide
CRISPR
screening,
we
identified
MALT1
as
regulator
protein.
Inhibition
expression
enhances
ubiquitination-mediated
degradation
up-regulating
E3
ubiquitin
ligase
RC3H1.
Using
both
rescue
assays
and
functional
genetic
demonstrate
that
pharmacologically
targeting
triggers
ferroptosis
liver
cells.
Moreover,
show
synergizes
with
sorafenib
or
regorafenib
to
induce
across
multiple
types.
These
findings
elucidate
modulatory
effects
MALT1-RC3H1
axis
on
stability,
revealing
molecular
mechanism
could
be
exploited
Open Medicine,
Journal Year:
2025,
Volume and Issue:
20(1)
Published: Jan. 1, 2025
This
study
aims
to
investigate
the
role
and
mechanism
of
p-hydroxyl
cinnamaldehyde
(CMSP)
in
triggering
ferroptosis
small
cell
lung
cancer
(SCLC)
cells.
The
impact
CMSP
on
H1688
SW1271
cells
was
assessed
through
experiments
biological
information
analysis.
Moreover,
expression
heme
oxygenase
1
(HMOX1)
SCLC
tissue
examined.
Following
treatment,
a
concentration-dependent
increase
death
observed,
differentially
expressed
genes
were
found
be
associated
with
ferroptosis.
notably
facilitated
events,
such
as
elevated
levels
reactive
oxygen
species
(ROS),
Fe2+,
malondialdehyde
(MDA),
transferrin
receptor
(TFR1),
divalent
metal
transporter
(DMT1),
decreased
glutathione
(GSH),
solute
carrier
family
7
member
11
(SLC7A11),
peroxidase
4
(GPX4).
Furthermore,
promoted
mitochondrial
dysfunction,
manifested
reduced
volume,
increased
membrane
density,
ROS,
potential.
Consistently,
mitochondrial-targeted
antioxidant
Mito-TEMPO
reversed
CMSP-induced
Expression
HMOX1
gene
markedly
under
while
lower
observed
compared
adjacent
tissue.
triggers
dysfunction
via
activation,
leading
cells,
underscoring
its
potential
therapeutic
agent
for
SCLC.
Cell Death and Disease,
Journal Year:
2025,
Volume and Issue:
16(1)
Published: Jan. 18, 2025
As
a
novel
form
of
nonapoptotic
cell
death,
ferroptosis
is
developing
into
promising
therapeutic
target
dedifferentiating
and
therapy-refractory
cancers.
However,
its
application
in
pancreatic
cancer
still
unknown.
In
the
preliminary
research,
we
found
that
F-box
WD
repeat
domain-containing
7
(FBW7)
inhibited
migration
proliferation
cells
through
substrate
c-Myc.
We
further
another
key
FBW7,
KLF5,
could
inhibit
ferroptosis.
Inhibiting
KLF5
significantly
enhances
cytotoxicity
oxaliplatin
rather
than
other
chemotherapy
drugs.
Mechanistically,
expression
heme
oxygenase
1
(HMOX1)
via
repressing
zinc
finger
E-box-binding
homeobox
(ZEB1).
Inhibition
facilitated
cytotoxic
effect
promoting
Oxaliplatin
combined
with
inhibitor
potentiated
death
vitro
tumor
growth
vivo
compared
either
treatment
alone.
These
results
reveal
critical
role
sensitized
cancer,
suggest
platinum-based
gemcitabine-based
expected
to
bring
better
effects.