Scientific Reports,
Год журнала:
2025,
Номер
15(1)
Опубликована: Янв. 13, 2025
Osteosarcoma
(OS)
is
the
most
common
primary
bone
malignancy.
The
canonical
Wnt
inhibitor
Dickkopf-1
(Dkk-1)
has
been
implicated
in
destruction,
tumor
survival
and
metastases
during
OS.
We
examined
role
of
Dkk-1
OS
disease
progression
explored
strategies
for
targeting
its
activity.
enhances
by
amplifying
a
non-canonical
pathway
that
upregulates
aldehyde
dehydrogenase
1A1.
Targeting
transcription
with
vivo
morpholino
(DkkMo)
reduced
enhanced
osteogenic
activity
vitro.
DkkMo
as
single
agent
slowed
expansion,
increased
necrosis,
inhibited
preserved
PDX
model
also
frequency
dividing
cells
reinitiated
regenerative
phenotype
tumors
stroma
while
reducing
infiltration
inflammatory
cells.
These
findings
indicate
potential
to
safely
target
osteosarcoma
growth,
survival,
destruction.
Proteomes,
Год журнала:
2025,
Номер
13(1), С. 7 - 7
Опубликована: Фев. 3, 2025
Background:
The
purpose
of
this
study
was
to
detect
proteomic
alterations
and
corresponding
signaling
pathways
involved
in
the
formation
age-related
cataract
(ARC),
diabetic
(DC),
post-vitrectomy
(PVC).
Methods:
Three
sample
types,
aqueous
humor
(AH),
anterior
capsule
(AC),
content
phaco
cassette,
were
collected
during
phacoemulsification
surgery.
samples
obtained
from
12
participants
without
diabetes
mellitus
(DM),
11
with
DM,
7
a
history
vitrectomy
surgery
past
months.
Sp3
protocol
(Single-Pot,
Solid-Phase,
Sample-Preparation)
used
for
preparation.
recognition
quantification
proteins
carried
out
liquid
chromatography
online
tandem
mass
spectrometry.
DIA-NN
software
applied
identification
peptides/proteins.
Statistical
analysis
data
visualization
conducted
on
Perseus
software.
Data
are
available
via
ProteomeXchange.
Results:
A
very
rich
atlas
lens
AH
proteome
has
been
generated.
Glycosaminoglycan
biosynthesis
non-canonical
Wnt
receptor
pathway
differentially
expressed
ARC
compared
both
DC
PVC
groups.
In
group,
complement
activation
samples,
while
glutathione
metabolism
oxidoreductase
activity
AC
samples.
Microfilament
motor
activity,
microtubule
cytoskeleton
organization,
binding
groups
Conclusions:
results
expand
existing
knowledge
pathophysiology
cataract,
suggest
possible
important
druggable
targets
slower
progression
or
even
prevention
cataract.
Future Oncology,
Год журнала:
2025,
Номер
unknown, С. 1 - 21
Опубликована: Фев. 12, 2025
Triple-negative
breast
cancer
(TNBC)
presents
a
formidable
global
health
challenge,
marked
by
its
aggressive
behavior
and
significant
treatment
resistance.
This
subtype,
devoid
of
estrogen,
progesterone,
HER2
receptors,
largely
relies
on
stem
cells
(BCSCs)
for
progression,
metastasis,
recurrence.
BCSCs,
characterized
their
self-renewal
capacity
resistance
to
conventional
therapies,
exploit
key
surface
markers
critical
signaling
pathways
like
Wnt,
Hedgehog,
Notch,
TGF-β,
PI3K/AKT/mTOR
Hippo-YAP/TAZ
thrive.
Their
adaptability
is
underscored
mechanisms
including
drug
efflux
enhanced
DNA
repair,
contributing
poor
prognosis
high
recurrence
rates.
The
tumor
microenvironment
(TME)
further
facilitates
BCSC
survival
through
complex
interactions
with
stromal
immune
cells.
Emerging
therapeutic
strategies
targeting
BCSCs
-
ranging
from
immunotherapy
nanoparticle-based
delivery
systems
gene-editing
technologies
aim
disrupt
these
resistant
Additionally,
innovative
approaches
focusing
exosome-mediated
metabolic
reprogramming
show
promise
in
overcoming
chemoresistance.
By
elucidating
the
distinct
characteristics
role
TNBC,
researchers
are
paving
way
novel
treatments
that
may
effectively
eradicate
resilient
cells,
mitigate
ultimately
improve
patient
outcomes.
review
highlights
urgent
need
targeted
address
unique
biology
pursuit
more
effective
interventions
TNBC.
Molecular Carcinogenesis,
Год журнала:
2025,
Номер
unknown
Опубликована: Март 18, 2025
ABSTRACT
Diffuse
large
B‐cell
lymphoma
(DLBCL)
is
the
most
prevalent
form
of
lymphoma.
The
overexpression
CtBP2
in
tissues
may
contribute
to
tumor
occurrence
and
progression.
expression
EGR1
DLBCL
elevated,
suggesting
its
potential
role
as
an
oncogene
that
promotes
proliferation
cells.
Database
predictions
indicate
can
bind
EGR1.
objective
present
study
was
investigate
whether
influence
apoptosis
cells
by
regulating
Wnt
signaling
pathway
through
Western
blot
assay
showed
upregulated
Cell
level
detected
CCK8
EdU
staining,
cycle
distribution
were
analyzed
flow
cytometry.
Our
data
indicated
interference
with
inhibit
cell
progression
while
promoting
apoptosis.
from
HDOCK
server,
along
results
Co‐IP
experiments,
suggested
effectively
each
other,
positioned
downstream
regulated
it.
Furthermore,
could
also
Wnt/β‐catenin
pathway.
Overexpression
counteracted
effects
siRNA‐CtBP2,
cycle,
inhibiting
upregulating
From
above
we
found
regulate
Therefore,
be
one
key
contributors
involved
regulation
CtBP2.
BMC Molecular and Cell Biology,
Год журнала:
2025,
Номер
26(1)
Опубликована: Апрель 29, 2025
Esophageal
squamous
cell
carcinoma
(ESCC),
one
of
the
most
aggressive
carcinomas
gastrointestinal
tract,
is
sixth
common
cause
cancer-related
death.
Wnt
pathway
plays
a
pivotal
role
in
proliferation
and
differentiation.
PYGO2
IL10
are
involved
this
pathway.
Our
aim
study
was
to
examine
correlation
between
expression
ESCC
patients
lines.
Relative-comparative
real
time-PCR
(RT-qPCR)
used
evaluate
mRNA
profile
58
non-treated
compared
their
margin
normal
tissues.
Expression
induced
KYSE-30
YM1
lines
analyzed.
The
results
revealed
significant
overexpression
31.0%
51.7%
ESCCs,
respectively.
significantly
correlated
each
other
(p
=
0.007).
Concomitant
genes
associated
grade
tumor
differentiation
<
0.01),
depth
invasion
0.05).
Induced
caused
meaningful
change
cells.
may
regulate
through
Wnt/β-catenin
signaling
pathway,
suggesting
possible
oncogenic
for
PYGO2/IL10
axis
tumorigenesis.
Considering
involvement
as
an
anti-inflammatory
cytokine
elevated
metastasis,
functional
interaction
these
factors
promote
process
which
induces
malignant
phenotype
ESCC.
Neuro-oncological
ventral
antigen
1
(NOVA1)
is
a
neuron-specific
RNA-binding
protein
which
regulates
alternative
splicing
in
the
developing
nervous
system.
Recent
research
has
found
that
NOVA1
plays
significant
role
carcinogenesis.
In
this
paper,
we
examine
of
non-small
cell
lung
cancer
(NSCLC)
and
its
underlying
molecular
mechanisms.The
expression
NSCLC
was
detected
by
immunohistochemistry
correlations
between
clinicopathological
factors
were
analyzed
chi-square
tests.
Kaplan-Meier
survival
analysis
Cox
regression
model
used
to
evaluate
predictive
effect
prognostic
factors.
Western
blotting,
Cell
Counting
Kit-8,
colony
formation,
apoptosis,
migration
invasion
assays
detect
effects
silencing
(si)NOVA1
RNA
on
Wnt/β-catenin
signaling
biological
behavior
lines.Our
study
showed
up-regulated
significantly
correlated
with
poor
differentiation
(p
=
0.020),
advanced
TNM
stage
(P
0.001),
T
0.001)
lymph
node
metastasis
0.000)
as
well
β-catenin
0.012)
NSCLC.
The
down-regulation
siRNA
inhibited
proliferation,
promoted
apoptosis
cells.
Expression
Wnt
molecules,
including
β-catenin,
activated
cyclin
D1,
matrix
metalloproteinase
(MMP)-2
MMP-7,
also
reduced
siNOVA1.
inhibition
A549
H1299
cells
siNOVA1
reversed
after
treatment
plasmid.The
present
suggests
may
serve
potential
prognosis
biomarker
High
associated
rate.
Finally,
vitro
experiments
verified
promotes
proliferation
regulating
signaling.
Molecular Therapy — Nucleic Acids,
Год журнала:
2021,
Номер
25, С. 455 - 467
Опубликована: Июнь 24, 2021
Non-coding
RNAs
play
essential
roles
in
breast
cancer
progression
by
regulating
proliferation,
differentiation,
invasion,
and
metastasis.
However,
our
understanding
of
most
microRNAs
(miRNAs)
long
noncoding
(lncRNAs)
is
still
limited.
miR-586
has
been
identified
as
an
important
factor
the
some
types
cancer,
but
its
exact
function
relative
regulation
mechanisms
development
need
to
be
further
investigated.
In
this
study,
we
showed
functioned
oncogene
promoting
proliferation
metastasis
both
vitro
vivo.
Meanwhile,
induced
Wnt/β-catenin
activation
directly
targeting
signaling
antagonists
SFRP1
DKK2/3.
Moreover,
demonstrated
that
LINC01189
a
tumor
suppressor
inhibited
through
inhibiting
epithelial-mesenchymal
transition
(EMT)-like
phenotype
sponging
miR-586.
addition,
β-catenin/TCF4
transactivated
ZEB1,
resulting
transcriptional
repression
expression.
conclusion,
data
uncovered
LINC01189-miR-586-ZEB1
feedback
loop
provided
novel
mechanism
participating
progression.