Al-Azhar Assiut Medical Journal,
Год журнала:
2024,
Номер
22(3), С. 151 - 157
Опубликована: Июль 1, 2024
Background
and
aim
Hepatocellular
carcinoma
(HCC)
is
the
sixth
most
common
cancer
worldwide
early
detection
can
improve
prognosis,
in
this
study,
we
aimed
to
investigate
hepatocyte
growth
factor
(HGF)
as
a
biomarker
for
of
HCC
post
hepatitis
C
liver
cirrhosis.
Patients
methods
In
measured
serum
HGF
alpha-fetoprotein
(AFP)
106
persons
who
were
divided
into
three
groups
group
(36
patients),
cirrhotic
(40
patients
had
virus
cirrhosis),
control
(30).
Results
levels
significantly
higher
than
Cirrhotic
group.
Also,
diagnose
with
sensitivity
specificity
96.9%
98.2%
at
more
426
pg/ml
compared
AFP
which
was
95%
90%
9.9
ng/ml.
Conclusion
may
be
crucial
marker
predicting
stages
AFP.
Signal Transduction and Targeted Therapy,
Год журнала:
2025,
Номер
10(1)
Опубликована: Фев. 6, 2025
Abstract
Liver
cancer
represents
a
major
global
health
concern,
with
projections
indicating
that
the
number
of
new
cases
could
surpass
1
million
annually
by
2025.
Hepatocellular
carcinoma
(HCC)
constitutes
around
90%
liver
and
is
primarily
linked
to
factors
incluidng
aflatoxin,
hepatitis
B
(HBV)
C
(HCV),
metabolic
disorders.
There
are
no
obvious
symptoms
in
early
stage
HCC,
which
often
leads
delays
diagnosis.
Therefore,
HCC
patients
usually
present
tumors
advanced
incurable
stages.
Several
signaling
pathways
dis-regulated
cause
uncontrolled
cell
propagation,
metastasis,
recurrence
HCC.
Beyond
frequently
altered
therapeutically
targeted
receptor
tyrosine
kinase
(RTK)
involved
differentiation,
telomere
regulation,
epigenetic
modification
stress
response
also
provide
therapeutic
potential.
Investigating
key
their
inhibitors
pivotal
for
achieving
advancements
management
At
present,
primary
approaches
(TKI),
immune
checkpoint
(ICI),
combination
regimens.
New
trials
investigating
therapies
involving
ICIs
TKIs
or
anti-VEGF
(endothelial
growth
factor)
therapies,
as
well
combinations
two
immunotherapy
The
outcomes
these
expected
revolutionize
across
all
Here,
we
here
comprehensive
review
cellular
pathways,
potential,
evidence
derived
from
late-stage
clinical
discuss
concepts
underlying
earlier
trials,
biomarker
identification,
development
more
effective
therapeutics
Research Square (Research Square),
Год журнала:
2025,
Номер
unknown
Опубликована: Янв. 1, 2025
Abstract
Hepatocellular
carcinoma
(HCC)
is
a
life-threatening
disease
with
global
impact,
underscoring
the
urgent
need
for
development
of
new
therapeutic
agents.
This
study
evaluates
effect
selenium-hydroxytyrosol
nanoparticles
(Se-HTNPs)
in
rat
model
HCC
induced
by
diethylnitrosamine
(DEN).
In
vitro,
Se-HTNPs
treatment
reduced
viability
Hep
G2
cells
dose-dependent
manner,
an
IC50
value
61.29
±
1.12
µg/mL.
The
results
confirmed
antioxidant,
anti-inflammatory,
and
anti-carcinogenic
properties
Se-HTNPs,
demonstrating
their
effectiveness
against
DEN-induced
HCC.
effects
were
validated
inhibiting
serum
ALT,
AST,
ALP
enzyme
activities
reducing
total
bilirubin
levels.
Simultaneously,
enhanced
albumin
protein
Additionally,
alleviated
oxidative
stress
significantly
lowering
hepatic
lipid
peroxidation
(MDA)
levels
markedly
increasing
antioxidant
marker
(GSH,
SOD,
TAC)
compared
to
DEN-administered
rats.
also
inflammatory
markers
(TNFα,
IL-6,
IL-1β),
apoptotic
(p53
caspase
3),
VEGF
Furthermore,
DEN
group,
distinctly
suppressed
c-JNK
mRNA
NF-κB
gene
expression
Moreover,
Se-HTNP
improved
histological
alterations
DEN.
conclusion,
these
findings
suggest
that
mitigate
rats
through
potent
properties.
Cell Death and Disease,
Год журнала:
2025,
Номер
16(1)
Опубликована: Фев. 17, 2025
Abstract
BRD1
encodes
a
protein
containing
bromodomain,
which
is
an
essential
component
of
histone
acetyltransferase
(HAT)
complexes.
These
complexes
play
crucial
role
in
the
regulation
gene
transcription
and
modification
chromatin
structures.
The
aberrant
expression
frequently
observed
across
range
cancer
types,
including
hepatocellular
carcinomas
(HCC).
However,
precise
mechanisms
through
contributes
to
tumorigenesis,
especially
HCC,
remain
unclear.
In
our
investigation,
we
have
uncovered
novel
for
as
oncogene
implicated
lipid
metabolism
HCC
progression.
Specifically,
deficiency
impedes
proliferation
metastasis
cells
reducing
accumulation
droplets
cholesterol
levels.
This
effect
mediated
SREBF1-induced
downregulation
SCD1
cells.
Mechanistically,
ablation
disrupts
acetylation
level
H3K9,
culminating
subsequent
trimethylation
H3K9
(H3K9me3).
Notably,
H3K14ac
partially
colocalizes
with
H3K9me3
its
methyltransferase
SETDB1
from
double
labeling
both
at
SREBF1
promoter.
creation
repressive
environment,
ultimately
leading
HCC.
Furthermore,
combinatorial
use
inhibitor
simvastatin
augments
antitumor
efficacy
vivo.
Collectively,
findings
underscore
critical
regulator
SREBF1-associated
participant
progression
distinct
epigenetic
regulatory
mechanism.
discoveries
further
suggest
promising
therapeutic
approach
treatment
Frontiers in Pharmacology,
Год журнала:
2025,
Номер
16
Опубликована: Фев. 21, 2025
Antibody-drug
conjugates
have
emerged
as
a
promising
cancer
treatment,
combining
targeted
delivery
of
cytotoxic
agents
with
the
specificity
monoclonal
antibodies.
Despite
their
potential,
ADCs
face
limitations
such
resistance
and
off-target
effects.
To
enhance
efficacy,
are
increasingly
being
combined
other
therapeutic
strategies,
including
immune
checkpoint
inhibitors,
chemotherapy,
small-molecule
anti-angiogenic
agents,
CAR-T
cell
therapies.
These
combination
therapies
aim
to
overcome
mechanisms,
improve
tumor
targeting,
boost
responses.
Clinical
studies
shown
that
combinations
can
significantly
response
rates
progression-free
survival
across
various
cancers.
This
review
explores
clinical
key
studies,
challenges,
future
perspectives
in
therapy.
World Journal of Surgical Oncology,
Год журнала:
2025,
Номер
23(1)
Опубликована: Март 29, 2025
Neuropilin
and
tolloid-like
2
(NETO2)
facilitates
the
progression
of
various
cancers,
but
its
role
in
hepatocellular
carcinoma
(HCC)
is
not
known.
This
study
aimed
to
assess
potential
targeting
NETO2
HCC
relationship
with
STAT3/C-MYC
pathway.
cells
(Huh7
MHCC-97
H)
were
cultured
transfected
control
siRNA
(siCtrl),
(siNETO2),
overexpression
(oeCtrl),
or
(oeNETO2),
non-transfected
used
as
blank
controls.
mRNA
protein
expressions
reduced
both
Huh7
H
cells.
EdU
CCK-8
assays
indicated
that
cell
proliferation
was
decreased
after
siNETO2
transfection
TUNEL
assay
found
revealed
apoptosis
rate
greater
cells,
tended
be
(but
difference
statistically
significant).
Transwell
invasion
number
invasive
transfection.
Cell
scratch
migration
significantly
different
Western
blotting
p-STAT3
C-MYC
Overexpression
experiments
promoted
oeNETO2
knockdown
suppresses
proliferation,
invasion,
inactivates
pathway,
suggesting
a
target
for
treatment.
