GluOC Induced SLC7A11 and SLC38A1 to Activate Redox Processes and Resist Ferroptosis in TNBC
Jiaojiao Xu,
No information about this author
Xue Bai,
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Keting Dong
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et al.
Cancers,
Journal Year:
2025,
Volume and Issue:
17(5), P. 739 - 739
Published: Feb. 21, 2025
Background/Objectives:
Ferroptosis,
a
type
of
programmed
cell
death,
is
mainly
associated
with
disruptions
in
iron
metabolism,
imbalances
the
amino
acid
antioxidant
system,
and
build-up
lipid
peroxides.
Triple-negative
breast
cancer
(TNBC)
has
dismal
prognosis.
Since
activating
ferroptosis
can
suppress
proliferation,
it
holds
promise
as
novel
therapeutic
target
for
patients.
Thus,
objective
this
study
was
to
clarify
mechanism
TNBC,
aiming
find
new
treatment
strategies
TNBC
Methods:
We
screened
out
differential
genes
related
after
GluOC
based
on
whole-genome
sequencing
results.
At
cellular
level,
we
conducted
explorations
using
techniques
such
quantitative
real-time
polymerase
chain
reaction
(qRT-PCR),
Western
blotting,
fluorescence
staining,
siRNA
transfection.
Moreover,
further
verified
role
inhibiting
through
vivo
experiments
nude
mice.
Results:
The
results
showed
that
enhanced
glutathione
expression
levels
by
inducing
SLC7A11
accumulation
via
specific
signaling
pathway.
Additionally,
increased
ATP
production
tricarboxylic
flux
resistance
SLC38A1.
Overall,
coordinately
regulated
SLC38A1
inhibit
TNBC.
Conclusions:
This
elucidated
findings
not
only
provided
insights
into
but
also
potentially
offered
concepts
development
future
anticancer
therapies,
which
may
contribute
improving
Language: Английский
Sodium butyrate increases USP5-mediated ubiquitination degradation of GPX4 and enhances anti-cancer efficacy of anti-PD-1 antibody
Qimeng Chang,
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Huarong Mao,
No information about this author
Jin-Feng Feng
No information about this author
et al.
Biochemical Pharmacology,
Journal Year:
2025,
Volume and Issue:
unknown, P. 116927 - 116927
Published: April 1, 2025
Language: Английский
A novel benzofuran derivative of β-elemene (ZT-22) inhibits hepatocellular carcinoma cell growth via directly targeting HSPA6
Zhiqiang Luo,
No information about this author
Huixia Fan,
No information about this author
Tao Zhang
No information about this author
et al.
Chemico-Biological Interactions,
Journal Year:
2025,
Volume and Issue:
unknown, P. 111514 - 111514
Published: April 1, 2025
Language: Английский
The deubiquitinase OTUD5 stabilizes SLC7A11 to promote progression and reduce paclitaxel sensitivity in triple-negative breast cancer
Cancer Letters,
Journal Year:
2024,
Volume and Issue:
604, P. 217232 - 217232
Published: Sept. 12, 2024
Language: Английский
Deubiquitinases as novel therapeutic targets for diseases
Yali Xian,
No information about this author
Jing Ye,
No information about this author
Yu Tang
No information about this author
et al.
MedComm,
Journal Year:
2024,
Volume and Issue:
5(12)
Published: Dec. 1, 2024
Deubiquitinating
enzymes
(DUBs)
regulate
substrate
ubiquitination
by
removing
ubiquitin
or
cleaving
within
chains,
thereby
maintaining
cellular
homeostasis.
Approximately
100
DUBs
in
humans
counteract
E3
ligases,
finely
balancing
and
deubiquitination
processes
to
maintain
proteostasis
respond
various
stimuli
stresses.
Given
their
role
modulating
levels
of
substrates,
are
increasingly
linked
human
health
disease.
Here,
we
review
the
DUB
family,
highlighting
distinctive
structural
characteristics
chain-type
specificities.
We
show
that
family
members
key
signaling
pathways,
such
as
NF-κB,
PI3K/Akt/mTOR,
MAPK,
play
crucial
roles
tumorigenesis
other
diseases
(neurodegenerative
disorders,
cardiovascular
diseases,
inflammatory
developmental
diseases),
making
them
promising
therapeutic
targets
Our
also
discusses
challenges
developing
inhibitors
underscores
critical
cancer.
This
comprehensive
analysis
enhances
our
understanding
complex
biological
functions
potential.
Language: Английский
USP24 promotes hepatocellular carcinoma tumorigenesis through deubiquitinating and stabilizing TRAF2
Biochemical Pharmacology,
Journal Year:
2024,
Volume and Issue:
229, P. 116473 - 116473
Published: Aug. 9, 2024
Ubiquitin-specific
peptidase
24
(USP24),
a
member
of
the
deubiquitinase
family,
plays
an
important
role
in
tumor
regulation.
However,
USP24
Hepatocellular
carcinoma(HCC)is
unknown.
The
aim
our
study
was
to
explore
HCC
seek
new
therapeutic
targets
for
HCC.
In
this
study,
we
found
that
aberrantly
upregulated
tissues
and
predicted
poor
prognosis.
markedly
promoted
proliferation
progression
vitro
vivo.
Mechanistically,
binds
necrosis
factor
receptor-associated
2(TRAF2)
inhibits
its
degradation,
thereby
promoting
accumulation
TRAF2.
Upregulation
TRAF2
activated
protein
kinase
B/nuclear
kappa-B
(AKT/
NF-κB)
signaling
pathway
cell
survival.
addition,
positively
correlated
with
programmed
death
ligand
1(PD-L1)
expression
HCC,
highlighting
clinical
significance
activation
immune
evasion.
Deletion
enhanced
tumor-killing
ability
CD8
Language: Английский