ONCOLOGIE,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Nov. 18, 2024
Abstract
Objectives
The
effect
of
exosome-derived
miR-21-5p
from
gastric
cancer
(GC)
on
angiogenesis
remains
unclear.
This
study
aims
to
examine
the
angiogenic
impact
GC
miR-21-5p.
Methods
Exosomes
were
isolated
cells
and
co-cultured
with
human
umbilical
vein
endothelial
(HUVECs).
levels
in
HUVECs
measured
by
qPCR.
Flow
cytometry
was
used
assess
apoptosis,
Cell
Counting
Kit-8
cell
growth.
Bioinformatics
analysis
identify
target
genes,
which
then
verified
dual-luciferase
gene
reporter
experiments.
qPCR
western
blotting
employed
expression
genes
proteins,
respectively.
Functional
rescue
assays
conducted
verify
that
regulates
function
targeting
LEM
domain
containing
3
(LEMD3).
Additionally,
migration
assessed
using
a
scratch
assay.
Results
Co-cultivation
GC-derived
exosomes
improved
survival,
decreased
raised
HUVECs.
Increases
vascular
growth
factor
A
(VEGFA)
TGF-β/Smad
signaling
pathway
seen.
It
shown
targets
LEMD3.
biological
effects
lessened
when
inhibited,
or
LEMD3
overexpressed.
Conclusions
By
LEMD3,
stimulates
triggering
cascade
upregulating
VEGFA
expression.
leads
increased
proliferation,
HUVECs,
underscoring
potential
this
therapy.
Military Medical Research,
Journal Year:
2025,
Volume and Issue:
12(1)
Published: Feb. 11, 2025
Abstract
Cancer
recurrence,
driven
by
the
phenomenon
of
tumor
dormancy,
presents
a
formidable
challenge
in
oncology.
Dormant
cancer
cells
have
ability
to
evade
detection
and
treatment,
leading
relapse.
This
review
emphasizes
urgent
need
comprehend
dormancy
its
implications
for
recurrence.
Despite
notable
advancements,
significant
gaps
remain
our
understanding
mechanisms
underlying
lack
reliable
biomarkers
predicting
provides
comprehensive
analysis
cellular,
angiogenic,
immunological
aspects
dormancy.
It
highlights
current
therapeutic
strategies
targeting
dormant
cells,
particularly
combination
therapies
immunotherapies,
which
hold
promise
preventing
By
elucidating
these
proposing
innovative
research
methodologies,
this
aims
deepen
ultimately
facilitating
development
more
effective
recurrence
improving
patient
outcomes.
World Journal of Surgical Oncology,
Journal Year:
2025,
Volume and Issue:
23(1)
Published: Jan. 28, 2025
The
clinical
benefits
of
neoadjuvant
bevacizumab
plus
chemotherapy
in
locally
advanced
gastric
cancer
patients
are
controversial.
This
study
intended
to
evaluate
the
efficacy
and
safety
these
patients.
In
this
retrospective
study,
71
receiving
or
alone
were
divided
into
chemo
group
(N
=
23)
48).
Objective
response
rate
(52.2%
vs.
35.4%),
disease
control
(91.3%
81.3%),
surgical
resection
(95.7%
85.4%),
R0
(87.0%
75.0%),
proportion
with
tumor
regression
grade
0–1
(31.8%
17.1%)
tended
increase
versus
group,
although
there
was
no
statistical
significance.
48-month
progression-free
survival
(PFS)
rates
58.3%
33.4%
group.
overall
(OS)
65.1%
46.5%
respectively.
PFS
ascend,
but
OS
did
not
vary
Bevacizumab
(vs.
chemo)
independently
related
longer
[hazard
ratio
(HR)
0.263,
P
0.015],
(HR
0.207,
0.056)
incidence
3–4
adverse
events
between
groups
(all
>
0.05).
Neoadjuvant
achieves
higher
treatment
some
extent,
tolerable
patients,
its
application
needs
further
verification.
Bioengineering-based
in
vitro
tumor
models
are
increasingly
important
as
tools
for
studying
disease
progression
and
therapy
response
many
cancers,
including
the
deadly
pancreatic
ductal
adenocarcinoma
(PDAC)
that
exhibits
a
tumor/tissue
microenvironment
of
high
cellular/biochemical
complexity.
Therefore,
it
is
crucial
to
capture
complexity
enable
investigation
interplay
between
cancer
cells
factors
such
extracellular
matrix
(ECM)
proteins
or
stroma
cells.
Using
polyurethane
(PU)
scaffolds,
we
performed
systematic
study
on
how
different
ECM
protein
scaffold
coatings
impact
long-term
cell
evolution
scaffolds
containing
only
(activated
stellate
endothelial
cells).
To
investigate
potential
further
changes
those
biomarkers
due
cancer-stroma
interactions,
mapped
their
expression
dual/zonal
consisting
core
periphery,
spatially
mimicking
fibrotic/desmoplastic
reaction
PDAC.
In
our
single
observed
coating
affected
spatial
aggregation,
deposition,
biomarker
upregulation
cell-line-dependent
manner.
levels
fibrosis/desmoplasia
terms
composition/quantity
were
generated
depending
coating.
When
model,
linked
aggressiveness/invasiveness
upregulated
by
both
compared
models.
Collectively,
advances
understanding
PU
scaffolds.
Our
findings
show
within
bioengineered
models,
can
stimulate
PDAC
develop
aggressiveness/invasiveness,
well
fibrosis.
Furthermore,
highlight
importance
considering
map
invasion.
work
contributes
design
with
variable,
yet
biomimetic,
tissue-like
properties
microenvironment's
role
progression.
Molecules,
Journal Year:
2025,
Volume and Issue:
30(6), P. 1201 - 1201
Published: March 7, 2025
Breast
cancer
(BC)
tops
the
list
of
causes
for
female
fatalities
globally,
with
elusive
triple-negative
breast
(TNBC)
constituting
10–20%
all
cases.
Current
clinical
strategies
combating
TNBC
encompass
a
multifaceted
approach,
including
surgical
intervention,
radiation
therapy,
chemotherapy,
and
advanced
targeted
drugs
immunotherapies.
While
these
modalities
have
catalyzed
significant
advancements
in
management,
lingering
limitations
continue
to
pose
formidable
challenges.
There
is
an
acute
need
novel
therapeutics
realm
treatment.
Natural
products
(NPs)
emerged
as
rich
reservoir
pharmaceutical
innovation,
owing
their
extraordinary
range
structures
physicochemical
properties.
Scholars
reported
diverse
evidence
NPs’
efficacy
against
TNBC.
This
review
aims
comprehensively
explore
bioactive
constituents,
specifics
commonalities
chemical
structure,
pharmacological
mechanisms
NPs,
specifically
examining
roles
impeding
which
recently
garnered
interest,
are
intriguing
terms
capacity
combat
through
mechanisms,
suppression
tumor
cell
proliferation,
induction
apoptosis,
inhibition
metastasis.
These
natural
agents
primarily
compounds,
terpenoids,
glycosides,
phenolic
alkaloids.
An
in-depth
exploration
has
unveiled
involvement
key
signaling
pathways,
transforming
growth
factor-beta
(TGF-β),
vascular
endothelial
factor
A
(VEGFA),
phosphoinositide
3-kinase/protein
kinase
B
(PI3K/AKT),
Wingless/Int-1
(Wnt)
/β-catenin,
mitogen-activated
protein
(MAPK)
pathways.
Meanwhile,
this
also
looks
at
challenges
opportunities
that
arise
from
harnessing
compounds
influence
TNBC,
while
outlining
prospective
trajectory
future
research
field
NPs.
MedComm,
Journal Year:
2025,
Volume and Issue:
6(4)
Published: March 30, 2025
ABSTRACT
Signal
transducer
and
activator
of
transcription
3
(STAT3)
is
a
critical
factor
involved
in
multiple
physiological
pathological
processes.
While
STAT3
plays
an
essential
role
homeostasis,
its
persistent
activation
has
been
implicated
the
pathogenesis
various
diseases,
particularly
cancer,
bone‐related
autoimmune
disorders,
inflammatory
cardiovascular
neurodegenerative
conditions.
The
interleukin‐6/Janus
kinase
(JAK)/STAT3
signaling
axis
central
to
activation,
influencing
tumor
microenvironment
remodeling,
angiogenesis,
immune
evasion,
therapy
resistance.
Despite
extensive
research,
precise
mechanisms
underlying
dysregulated
disease
progression
remain
incompletely
understood,
no
United
States
Food
Drug
Administration
(USFDA)‐approved
direct
inhibitors
currently
exist.
This
review
provides
comprehensive
evaluation
STAT3's
health
disease,
emphasizing
involvement
cancer
stem
cell
maintenance,
metastasis,
inflammation,
drug
We
systematically
discuss
therapeutic
strategies,
including
JAK
(tofacitinib,
ruxolitinib),
Src
Homology
2
domain
(S3I‐201,
STATTIC),
antisense
oligonucleotides
(AZD9150),
nanomedicine‐based
delivery
systems,
which
enhance
specificity
bioavailability
while
reducing
toxicity.
By
integrating
molecular
mechanisms,
pathology,
emerging
interventions,
this
fills
knowledge
gap
STAT3‐targeted
therapy.
Our
insights
into
crosstalk,
epigenetic
regulation,
resistance
offer
foundation
for
developing
next‐generation
with
greater
clinical
efficacy
translational
potential.
The
biofilm
functions
as
a
physical
barrier
for
bacteria,
enhancing
their
resistance
to
antibiotics
and
contributing
recurrent
infections.
Therefore,
the
scavenging
of
biofilms
has
become
an
important
strategy
treating
chronic
In
this
study,
we
demonstrated
that
Chlorella
pyrenoidosa
(CP)
downregulates
adhesion
genes
Staphylococcus
aureus
inhibits
formation.
Through
combination
CP
with
antibiotic
drug
berberine
hydrochloride
(BH)
stabilizers
(Poloxamer
188
Poloxamer
407),
developed
biologically
active
hydrogel
system,
which
termed
BHLip@CP
gel.
Under
laser
irradiation,
gel
generated
reactive
oxygen
species,
assisted
BH
effectively
inhibit
formation
in
S.
reduce
production
virulence
factors.
addition,
accelerated
wound
healing
infections
by
promoting
angiogenesis
skin
regeneration.
This
study
proposes
innovative
simultaneously
eliminate
bacterial
promote
via
synergistic
approach
combines
chemical
photodynamic
processes.
The FASEB Journal,
Journal Year:
2025,
Volume and Issue:
39(10)
Published: May 12, 2025
ABSTRACT
Tumor
angiogenesis
is
essential
for
further
growth
and
metastasis
of
solid
tumors.
However,
the
mechanisms
underlying
angiogenesis‐related
gene
expression
have
yet
to
be
clarified.
Here,
we
discovered
RNA‐binding
proteins
monocyte
chemotactic
protein‐induced
protein
2
(MCPIP2)
insulin‐like
factor
mRNA‐binding
1
(IGF2BP1)
function
as
a
pair
antagonists
that
modulate
breast
tumor
by
competitively
regulating
mRNA
stability
proangiogenic
transcripts,
including
vascular
endothelial
A
(
VEGFA
),
Erb‐B2
receptor
tyrosine
kinase
ERBB2
interleukin‐8
IL8
C‐X‐C
motif
chemokine
ligand
CXCL1
ephrin
A1
EFNA1
).
Mechanistically,
MCPIP2
physically
interacted
with
stem–loop
structures
in
3′‐untranslated
region
transcripts
through
its
RNase
domain
destabilize
their
mRNAs.
Ribosomal
might
required
MCPIP2‐mediated
destabilization
On
other
hand,
IGF2BP1
can
stabilize
mRNAs
binding
common
RNA
structures.
Furthermore,
found
human
tumors
was
repressed,
whereas
increased.
Lower
higher
were
significantly
associated
poor
survival
cancer
patients,
respectively.
Notably,
there
reversed
correlation
relationship
between
MCPIP2,
expression,
samples.
Collectively,
our
results
elucidate
novel
mechanism
which
provides
new
insights
into
antiangiogenic
therapy
cancer.