Molecular Carcinogenesis,
Год журнала:
2024,
Номер
unknown
Опубликована: Ноя. 8, 2024
Clear
cell
renal
carcinoma
(ccRCC)
is
characterized
by
its
aggressive
invasion
and
metastasis,
presenting
significant
clinical
challenges.
Gaining
insights
into
the
molecular
mechanisms
underlying
progression
crucial
for
development
of
effective
therapeutic
strategies.
Addressing
a
critical
knowledge
gap
in
understanding
ccRCC
tumorigenesis,
this
study
aims
to
elucidate
expression
patterns
TRIM21
ccRCC,
unravel
impact
on
patient
prognosis,
investigate
regulatory
role
ASS1
urea
cycle
dysregulation
within
context
ccRCC.
The
results
demonstrate
that
downregulated
low
predicts
an
unfavorable
prognosis
patients.
Furthermore,
upregulation
can
inhibit
migration
cells
regulating
ubiquitination
modification
ASS1.
This
not
only
expands
functional
tumorigenesis
but
also
demonstrates
ability
reverse
through
stabilizing
expression.
Specifically,
abnormal
downregulation
reduces
K63
ASS1,
leading
decreased
stability
protein,
aggravated
dysregulation,
facilitated
cells.
Additionally,
reduction
reverses
depressed
caused
overexpression
In
summary,
our
findings
contribute
deeper
played
progression,
pinpoint
unique
novel
mechanism
involving
ectopic
downregulation-mediated
dysfunction
during
provide
fresh
further
investigation
pathogenesis
metabolic
reprogramming
associated
with
Sophocarpine
(SC)
has
been
reported
to
suppress
tumorigenesis.
But
the
effect
of
SC
on
glioblastoma
(GBM)
is
unknown.
This
study
explored
anti-proliferation
and
pro-apoptosis
effects
GBM
cells
molecular
mechanism.
Different
concentrations
were
used
treat
human
astrocyte
NHA
lines
LN229
SF539.
CCK-8
was
applied
analyze
cell
toxicity
proliferation.
qRT-PCR
western
blot
measure
RNA
protein
expressions,
respectively.
Cell
cycle
apoptosis
determined
by
flow
cytometry
assay.
The
results
indicated
that
inhibited
proliferation
induced
SF539
in
a
dose-dependent
manner.
arrest
G0/G1
phase
increased
after
treatment.
Moreover,
downregulated
miR-21
expression
upregulated
PTEN
cells.
Overexpression
partly
abrogated
cells,
while
exogenous
partially
eliminated
pro-proliferation
anti-apoptosis
Furthermore,
treatment
decreased
levels
PI3K/AKT
pathway-related
p-PI3K,
p-AKT
PIP3
pathway
activator
740Y-P
reversed
reduced
enhanced
SC-treated
Significantly,
we
verified
suppressed
via
inhibiting
it
not
entirely
dependent
upregulation
PTEN.
Consequently,
potential
mechanism
induction
verified,
which
might
provide
new
method
for
PLoS ONE,
Год журнала:
2025,
Номер
20(1), С. e0317454 - e0317454
Опубликована: Янв. 17, 2025
Primary
hepatocellular
carcinoma
(PHC)
is
the
sixth
most
common
cancer
and
third
leading
cause
of
death
worldwide.
Hepatocellular
(HCC)
accounts
for
75%-85%
PHC.
LARP3
aberrantly
expressed
in
multiple
cancers.
We
found
that
it
significantly
highly
liver
tissues
HCC
patients,
but
exact
role
specific
mechanism
this
abnormal
expression
are
not
yet
clear.
In
study,
through
bioinformatics
analysis,
we
concluded
associated
with
a
poor
prognosis
patients
HCC.
Through
cellular
experiments
such
as
gene
editing
phenotypic
functions,
promotes
occurrence
development
inhibits
apoptosis.
Finally,
biological
means
RNA
sequencing,
flow
cytometry,
western
blotting,
construction
subcutaneous
tumorigenesis
model
nude
mice,
inhibition
apoptosis
by
related
to
negatively
regulating
ROS
level
inhibiting
PI3K/c-Fos/apoptosis
axis.
This
study
will
provide
potential
targets
treatment
Frontiers in Pharmacology,
Год журнала:
2025,
Номер
16
Опубликована: Фев. 20, 2025
Renal
cancer
is
known
for
its
aggressive
progression
and
resistance
to
standard
treatments,
underscoring
the
need
novel
therapeutic
strategies.
This
study
explores
potential
of
combining
6-shogaol
(6-SHO),
a
bioactive
compound
derived
from
ginger
(Zingiber
officinale),
with
hyperthermia
enhance
anticancer
efficacy
in
ACHN
renal
cells.
cells
were
treated
6-SHO
exposed
hyperthermic
conditions.
We
evaluated
combined
effects
on
apoptosis,
cell
cycle
arrest,
proliferation,
as
well
role
reactive
oxygen
species
(ROS)
heat
shock
proteins
(HSPs)
mediating
these
responses.
The
combination
significantly
increased
induced
G2/M
phase
reduced
proliferation
more
effectively
than
either
treatment
alone.
ROS
played
critical
effects,
modulation
HSPs
factor
1
(HSF1)
further
disrupting
survival
mechanisms.
These
findings
highlight
synergistic
approach
treatment,
supporting
research
clinical
evaluation.
BMC Cardiovascular Disorders,
Год журнала:
2024,
Номер
24(1)
Опубликована: Май 5, 2024
Abstract
Background
This
study
was
designed
to
investigate
the
mechanism
by
which
miR-30a-5p
mediates
cardiomyocyte
apoptosis
after
acute
myocardial
infarction
(AMI)
induced
hypoxia/reoxygenation
(H/R).
Methods
Differentially
expressed
miRNAs
were
analyzed
RNA
high-throughput
sequencing
in
(ST-elevation
infarction)
patients
versus
healthy
individuals
(controls).
The
H/R
model
used
assess
regulatory
of
AMI.
Lentivirus-associated
vectors
overexpress
or
knock
down
cellular
models.
pathological
mechanisms
regulating
development
serially
explored
qPCR,
bioinformatics,
target
gene
prediction,
dual
luciferase,
enzyme-linked
immunosorbent
assays
(ELISAs)
and
Western
blotting.
Results
results
showed
that
expression
significantly
increased
AMI
H9C2
cells.
Hypoxia
decreased
survival
over
time,
reoxygenation
further
reduced
cell
survival.
Bax
Phosphatase
tensin
homolog
(PTEN)were
suppressed,
while
Bcl-2
upregulated.
Additionally,
specifically
targeted
PTEN
gene.
According
GO
KEGG
analyses,
may
participate
interacting
with
PTEN.
mimic
apoptosis-related
proteins
levels
proinflammatory
markers
IL-1β,
IL-6,
TNF-α
activating
PTEN/PI3K/Akt
signaling
pathway.
Conversely,
anti-miR-30a-5p
treatment
attenuated
these
effects.
silencing
had
opposite
effects
on
H/R-induced
apoptosis.
Conclusions
plays
a
crucial
role
hypoxia-induced
infarction.
Our
findings
provide
translational
evidence
is
novel
potential
therapeutic
for
Molecules,
Год журнала:
2024,
Номер
29(10), С. 2306 - 2306
Опубликована: Май 14, 2024
Methylglyoxal-induced
ROS
elevation
is
the
primary
cause
of
neuronal
damage.
Metformin
a
traditional
hypoglycemic
drug
that
has
been
reported
to
be
beneficial
nervous
system.
In
this
study,
flavonoids
were
found
enhance
protective
effect
metformin
when
added
at
molar
concentration
0.5%.
The
structure–activity
relationship
(SAR)
analysis
indicated
ortho-
substitution
in
B
ring,
and
absence
double
bonds
between
2
3
position
combined
with
gallate
R
configuration
C
ring
played
crucial
roles
synergistic
effects,
which
could
for
designing
combination
compounds.
Additionally,
mechanism
study
revealed
typical
flavonoid,
EGCG,
enhanced
scavenging
anti-apoptotic
ability
via
BCL2/Bax/Cyto
C/Caspase-3
pathway,
synergistically
inhibited
expression
GSK-3β,
BACE-1,
APP
PC-12
cells
used
metformin.
dose
was
only
1/4
conventional
alone.
These
results
suggested
ROS-mediated
apoptosis
pathways
related
amyloid
plaques
(Aβ)
formation
can
targets
neuroprotective
effects
Abstract
Non-small
cell
lung
cancer
(NSCLC)
is
one
of
the
most
common
malignant
tumors.
Chemicals
and
target-directed
therapy
have
been
used
to
treat
these
tumors,
but
development
resistance
has
hampered
patient
treatment.
Thus,
many
researchers
are
seeking
new
compounds
that
capable
reversing
resistance.
Plants
from
Brazilian
Amazon,
such
as
Apuleia
leiocarpa,
represent
an
alternative
source
with
potential
cancer.
Increasing
concentrations
A.
leiocarpa
extracts
(25,
50
100
µg/ml)
stem,
sapwood,
root,
stem
bark
were
tested
against
NSCLC
line
(H460)
for
48
h.
The
dichloromethane-stem
(ALE3)
ethanolic-stem
(ALE5)
inhibited
viability
further
evaluated
apoptosis,
loss
mitochondrial
membrane
(MMP),
expression
proteins
belonging
apoptotic
autophagic
pathway.
results
indicated
ALE3
ALE5
induced
dose-dependent
apoptosis
MMP,
while
markers
p53
active
caspase
3,
autophagy
Beclin-1,
ATG12
LC3II.
This
study
demonstrates
first
time
possess
significant
antitumoral
fight
