Phytomedicine,
Год журнала:
2024,
Номер
136, С. 156303 - 156303
Опубликована: Дек. 4, 2024
Abnormal
antioxidant
capacity
in
cancer
cells
is
intimately
linked
to
tumor
aggressiveness.
Modulating
oxidative
stress
status
and
inhibiting
ferroptosis
represents
a
novel
anticancer
therapeutic
strategy.
STAM
Binding
Protein
Like
1
(STAMBPL1),
deubiquitinase,
implicated
various
malignancies,
yet
its
function
potential
for
cholangiocarcinoma
(CCA)
remains
unexplored.
Redox Biology,
Год журнала:
2024,
Номер
75, С. 103259 - 103259
Опубликована: Июнь 27, 2024
Ferroptosis
is
a
form
of
iron-related
oxidative
cell
death
governed
by
an
integrated
redox
system,
encompassing
pro-oxidative
proteins
and
antioxidative
proteins.
These
undergo
precise
control
through
diverse
post-translational
modifications,
including
ubiquitination,
phosphorylation,
acetylation,
O-GlcNAcylation,
SUMOylation,
methylation,
N-myristoylation,
palmitoylation,
modification.
modifications
play
pivotal
roles
in
regulating
protein
stability,
activity,
localization,
interactions,
ultimately
influencing
both
the
buildup
iron
lipid
peroxidation.
In
mammalian
cells,
regulators
ferroptosis
typically
degradation
via
two
principal
pathways:
ubiquitin-proteasome
which
handles
majority
degradation,
autophagy,
primarily
targeting
long-lived
or
aggregated
This
comprehensive
review
aims
to
summarize
recent
advances
modification
linked
ferroptosis.
It
also
discusses
strategies
for
modulating
systems,
providing
new
insights
into
potential
therapeutic
applications
cancer
non-neoplastic
diseases.
Antioxidants,
Год журнала:
2024,
Номер
13(6), С. 697 - 697
Опубликована: Июнь 6, 2024
Glutathione
(GSH),
a
prominent
antioxidant
in
organisms,
exhibits
diverse
biological
functions
and
is
crucial
safeguarding
cells
against
oxidative
harm
upholding
stable
redox
milieu.
The
metabolism
of
GSH
implicated
numerous
diseases,
particularly
the
progression
malignant
tumors.
Consequently,
therapeutic
strategies
targeting
regulation
synthesis
to
modulate
levels
represent
promising
avenue
for
future
research.
This
study
aimed
elucidate
intricate
relationship
between
ferroptosis,
highlighting
how
modulation
can
impact
cellular
susceptibility
ferroptosis
consequently
influence
development
tumors
other
diseases.
paper
provides
comprehensive
overview
physiological
GSH,
including
its
structural
characteristics,
physicochemical
properties,
sources,
metabolic
pathways,
as
well
investigate
molecular
mechanisms
underlying
potential
interventions.
Unraveling
role
holds
promise
individuals
afflicted
with
European Journal of Pharmacology,
Год журнала:
2024,
Номер
972, С. 176553 - 176553
Опубликована: Апрель 2, 2024
Stroke
poses
a
significant
risk
of
mortality,
particularly
among
the
elderly
population.
The
pathophysiological
process
ischemic
stroke
is
complex,
and
it
crucial
to
elucidate
its
molecular
mechanisms
explore
potential
protective
drugs.
Ferroptosis,
newly
recognized
form
programmed
cell
death
distinct
from
necrosis,
apoptosis,
autophagy,
closely
associated
with
pathophysiology
stroke.
N6022,
selective
inhibitor
S-nitrosoglutathione
reductase
(GSNOR),
"first-in-class"
drug
for
asthma
therapeutic
applications.
However,
remains
unclear
whether
N6022
exerts
effects
in
stroke,
precise
action
are
unknown.
This
study
aimed
investigate
mitigates
cerebral
ischemia/reperfusion
(I/R)
injury
by
reducing
ferroptosis
underlying
mechanisms.
Accordingly,
we
established
an
oxygen-glucose
deprivation/reperfusion
(OGD/R)
model
middle
artery
occlusion/reperfusion
(MCAO/R)
mouse
mimic
I/R
injury.
Our
data,
both
vitro
vivo,
demonstrated
that
effectively
protected
against
I/R-induced
brain
damage
neurological
deficits
mice,
as
well
OGD/R-induced
BV2
damage.
Mechanistically,
promoted
Nrf2
nuclear
translocation,
enhancing
intracellular
antioxidant
capacity
SLC7A11-GPX4
system.
Furthermore,
interfered
interaction
GSNOR
GSTP1,
thereby
boosting
GSTP1
attenuating
ferroptosis.
These
findings
provide
novel
insights,
showing
attenuates
microglial
induced
through
promotion
translocation
inhibition
GSNOR/GSTP1
axis.
Frontiers in Pharmacology,
Год журнала:
2024,
Номер
15
Опубликована: Сен. 30, 2024
Cancer,
the
world’s
second
leading
cause
of
death
after
cardiovascular
diseases,
is
characterized
by
hallmarks
such
as
uncontrolled
cell
growth,
metastasis,
angiogenesis,
hypoxia,
and
resistance
to
therapy.
Autophagy,
a
cellular
process
that
can
both
support
inhibit
cancer
progression,
plays
critical
role
in
development
progression.
This
involves
formation
autophagosomes
ultimately
fuse
with
lysosomes
degrade
components.
A
key
regulator
this
Sirtuin
1
(SIRT1),
which
significantly
influences
autophagy.
review
delves
into
SIRT1
modulating
autophagy
its
broader
impacts
on
carcinogenesis.
regulates
crucial
mediators,
AMP-activated
protein
kinase
(AMPK)
mammalian
target
rapamycin
(mTOR),
effectively
promoting
or
suppressing
Beyond
direct
effects
autophagy,
SIRT1’s
regulatory
actions
extend
other
processes,
including
apoptosis
ferroptosis,
thereby
influencing
tumor
proliferation,
chemotherapy
responses.
These
insights
underscore
complex
interplay
between
significant
implications
for
Targeting
associated
pathways
presents
promising
strategy
manipulate
treatment.
underscores
potential
therapeutic
target,
opening
new
avenues
enhancing
treatment
efficacy.
Pharmacological Research,
Год журнала:
2024,
Номер
210, С. 107490 - 107490
Опубликована: Ноя. 5, 2024
The
emergence
of
sorafenib
resistance
has
become
a
predominant
impediment
and
formidable
dilemma
in
the
therapeutic
approach
for
hepatocellular
carcinoma
(HCC).
Although
approval
next-generation
drugs
as
alternatives
to
is
significant
development,
concurrent
use
inhibitors
that
target
additional
key
molecular
pathways
remains
an
effective
strategy
mitigate
acquisition
resistance.
Here,
we
identified
Glutathione
S-Transferase
Alpha
1
(GSTA1)
critical
modulator
(SR)
(HCC)
based
on
our
findings
from
experiments
conducted
recurrent
liver
cancer
tissues,
xenograft
mouse
models,
organoids,
sorafenib-resistant
cells.
Elevated
GSTA1
levels
are
strongly
associated
with
adverse
clinical
prognoses.
knockout
reinstates
sensitivity,
whereas
its
overexpression
attenuates
drug
efficacy.
Mechanistically,
enhances
accumulation
lipid
peroxides
suppresses
ferroptosis
by
exerting
peroxidase
function
regulate
SR.
Notably,
upregulation
expression
mediated
transcription
factor
CTNNB1
(β-catenin),
resulting
formation
cytoplasmic
complex
between
CTNNB1.
This
facilitates
nuclear
translocation
CTNNB1,
establishing
positive
feedback
loop.
combined
demonstrated
synergistic
anti-tumour
effects
through
induction
both
vitro
vivo.
Our
reveal
novel
regulatory
role
GSTA1/CTNNB1
axis
ferroptosis,
suggesting
targeting
could
be
promising
circumvent
HCC.
Heliyon,
Год журнала:
2024,
Номер
10(14), С. e34397 - e34397
Опубликована: Июль 1, 2024
Multiple
myeloma
(MM)
is
an
incurable
malignancy
of
plasma
cells
that
sensitive
to
T-5224,
AP-1
inhibitor.
Previous
study
indicated
T-5224
inhibits
proliferation
and
induces
apoptosis
in
MM
cells.
However,
the
high
mortality
cannot
be
fully
explained.
To
date,
no
studies
have
investigated
ferroptosis
induced
by
MM.
Therefore,
we
further
mechanism
which
kills
We
observed
exhibits
antimyeloma
properties
both
vitro
vivo.
T-5224-induced
cell
death
was
reversed
ferroptosis-specific
inhibitor
ferropstatin-1
(Fer-1).
The
protein
levels
key
regulators
GPX4
SLC7A11
were
decreased
Furthermore,
reduced
phosphorylation
PI3K
AKT
signaling
pathway
components,
ultimately
causing
death.
Using
740
Y–P,
a
activator,
Fer-1,
inhibitor,
discovered
through
PI3K/AKT
pathway.
Bortezomib
(BTZ),
FDA-approved
drug
for
treatment,
can
administered
combination
with
other
agents.
evaluated
synergistic
effect
BTZ
combined
inhibitors
on
Our
findings
provide
better
theoretical
basis
potential
new
perspective
treatment.