Frontiers in Bioscience-Landmark,
Год журнала:
2025,
Номер
30(3)
Опубликована: Март 5, 2025
Background:
The
CD47
molecule
(CD47)
performs
a
novel
role
in
regulating
immunoreactions
by
binding
to
signal-regulatory
protein
alpha
(SIRPα),
resulting
the
tumorigenesis
of
multiple
malignant
neoplasms.
However,
its
effects
and
mechanisms
breast
cancer
(BC)
remain
unknown.
Methods:
To
explore
molecular
explicit
impacts
CD47,
we
screened
two
databases
for
CD47-associated
signaling
pathways
cellular
functions.
BC
samples
patients’
basic
information
were
collected
identify
statistical
significance
expression.
We
also
constructed
experiments
validate
regulatory
cell
proliferation.
Results:
Analysis
TCGA-BRCA,
GSE42568,
GSE15852
datasets
demonstrated
an
elevated
level
tissues.
A
Venn
diagram
revealed
11,194
co-expressed
genes,
pathway
analysis
linked
levels
critical
pathways,
such
as
cytokine-receptor
interactions
Janus
kinase/signal
transducer
activator
transcription
(JAK/STAT)
signaling,
which
are
integral
proliferation
invasiveness.
Clinical
data
from
108
specimens
showed
that
localization
was
primarily
membranous,
with
higher
correlating
marker
Ki-67
(Ki-67)
expression
(p
<
0.0001)
advanced
tumor/node/metastasis
(TNM)
stage
0.0001).
Additionally,
functional
assays
depletion
reduced
viability
0.01),
migration
0.001),
invasion
0.05
4T1
cells;
p
0.001
MDA-MB-231
cells)
vitro
led
smaller
tumor
volumes
vivo.
Conclusion:
is
key
regulator
invasiveness
serves
potential
assessing
aggressiveness
guiding
therapeutic
strategies.
Metabolic
alterations,
a
hallmark
of
cancer,
enable
tumor
cells
to
adapt
their
environment
by
modulating
glucose,
lipid,
and
amino
acid
metabolism,
which
fuels
rapid
growth
contributes
treatment
resistance.
In
primary
breast
metabolic
shifts
such
as
the
Warburg
effect
enhanced
lipid
synthesis
are
closely
linked
chemotherapy
failure.
Similarly,
metastatic
lesions
often
display
distinct
profiles
that
not
only
sustain
but
also
confer
resistance
targeted
therapies
immunotherapies.
The
review
emphasizes
two
major
aspects:
mechanisms
driving
in
both
how
unique
environments
sites
further
complicate
treatment.
By
targeting
vulnerabilities
at
stages,
new
strategies
could
improve
efficacy
existing
provide
better
outcomes
for
cancer
patients.
Frontiers in Immunology,
Год журнала:
2025,
Номер
15
Опубликована: Янв. 8, 2025
Golgi
Protein
73
(GP73)
is
a
Golgi-resident
protein
that
highly
expressed
in
primary
tumor
tissues.
Initially
identified
as
an
oncoprotein,
GP73
has
been
shown
to
promote
development,
particularly
by
mediating
the
transport
of
proteins
related
epithelial-mesenchymal
transition
(EMT),
thus
facilitating
cell
EMT.
Though
our
previous
review
summarized
functional
roles
intracellular
signal
transduction
and
its
various
mechanisms
promoting
EMT,
recent
studies
have
revealed
plays
crucial
role
regulating
immune
microenvironment.
can
modulate
signaling
pathways
influence
cytokine
chemokine
networks,
resulting
inflammation
caused
viral
bacterial
infection
or
diseases,
leading
microenvironment
deteriorated.
Additionally,
extracellular
also
regulate
target
cells
binding
their
cell-surface
receptors
entering
acceptor
cells,
thereby
development.
In
this
review,
we
aim
summarize
findings,
providing
insights
for
future
investigations
on
potential
therapeutic
ameliorating
chronic
Cancers,
Год журнала:
2025,
Номер
17(2), С. 234 - 234
Опубликована: Янв. 13, 2025
The
complex
signaling
network
within
the
breast
tumor
microenvironment
is
crucial
for
its
growth,
metastasis,
angiogenesis,
therapy
escape,
stem
cell
maintenance,
and
immunomodulation.
An
array
of
secretory
factors
their
receptors
activate
downstream
cascades
regulating
cancer
progression
metastasis.
Among
various
pathways,
EGFR,
ER,
Notch,
Hedgehog
pathways
have
recently
been
identified
as
in
terms
proliferation,
survival,
differentiation,
maintenance
CSCs,
failure.
These
mediate
such
MAPK,
including
MEK/ERK
that
promote
common
pro-oncogenic
signaling,
whereas
dysregulation
PI3K/Akt,
Wnt/β-catenin,
JAK/STAT
activates
key
oncogenic
events
drug
resistance,
CSC
enrichment,
metabolic
reprogramming.
Additionally,
these
orchestrate
an
intricate
interplay
between
stromal
cells,
immune
cells.
Metabolic
reprogramming
adaptations
contribute
to
aggressive
are
unresponsive
therapy.
Herein,
recent
insights
into
novel
operating
TME
aid
advancement
emphasized
current
developments
practices
targeting
enhance
treatment
efficacy
reviewed.
Cancer Cell International,
Год журнала:
2024,
Номер
24(1)
Опубликована: Окт. 7, 2024
The
extracellular
matrix
(ECM)
is
a
complex,
dynamic
network
of
multiple
macromolecules
that
serve
as
crucial
structural
and
physical
scaffold
for
neighboring
cells.
In
the
tumor
microenvironment
(TME),
ECM
proteins
play
significant
role
in
mediating
cellular
communication
between
cancer-associated
fibroblasts
(CAFs)
tumor-associated
macrophages
(TAMs).
Revealing
modification
TME
necessitates
intricate
signaling
cascades
transpire
among
diverse
cell
populations
proteins.
advent
single-cell
sequencing
has
enabled
identification
refinement
specific
subpopulations,
which
substantially
enhanced
our
comprehension
milieu
given
us
high-resolution
perspective
on
diversity
However,
it
essential
to
integrate
data
establish
coherent
framework.
this
regard,
we
present
comprehensive
review
relationships
ECM,
TAMs,
CAFs.
This
encompasses
insights
into
released
by
TAMs
CAFs,
integration
TAM-ECM-CAF
axis,
potential
applications
limitations
targeted
therapies
serves
reliable
resource
focused
therapeutic
strategies
while
highlighting
intermediates
TME.
Frontiers in Pharmacology,
Год журнала:
2025,
Номер
15
Опубликована: Янв. 15, 2025
TRIB3
has
been
reported
to
mediate
breast
cancer
(BC)
proliferation
and
metastasis
by
interacting
with
AKT1,
blocking
the
interaction
between
AKT1
can
inhibit
progression
of
BC.
Besides,
inhibiting
turn
"cold
tumor"
hot
also
proved
be
an
effective
therapeutic
strategy
for
Thus,
this
study
aim
find
drugs
that
bind
BC
progression,
further
elucidate
its
mechanism.
The
possible
inhibitors
were
screened
high-throughput
molecular
docking,
CETSA,
CO-IP
assay.
Then,
effect
inhibitor
anti
was
assessed
CCK-8
assay,
flow
cytometry,
plate
colony
formation
transwell
assay;
RNA-seq
empolyed
potential
mechanism
Parishin
B
(PB)
anti-BC.
Finally,
on
lung
in
vivo
evaluated.
PB
as
a
TRIB3,
CETSA
assay
indicated
could
target
block
TRIB3-AKT1
interaction.
In
addition,
exhibited
good
anti-BC
activity
without
drug
toxicity
normal
cells
experiments
vitro,
analysis
suggested
invasion
related
cell
cycle.
It
vivo.
demonstrated
regulating
cycle,
providing
agent
treatment
Computer Methods in Biomechanics & Biomedical Engineering,
Год журнала:
2025,
Номер
unknown, С. 1 - 14
Опубликована: Янв. 27, 2025
Breast
cancer
(BC)
is
a
malignant
tumor
that
occurs
in
breast
tissue.
This
project
aims
to
predict
the
prognosis
of
BC
patients
using
genes
related
hypoxia
and
endoplasmic
reticulum
stress
(ERS).
RNA-seq
clinical
data
for
were
downloaded
from
TCGA
GEO
databases.
Hypoxia
ERS-related
collected
Genecards
database.
Univariate/multivariate
Cox
regression
Lasso
analyses
used
screen
construct
prognostic
models.
Patients
divided
into
high-risk
(HR)
low-risk
(LR)
groups
based
on
risk
scores.
The
CIBERSORT
algorithm
was
analyze
differences
immune
infiltration
between
two
groups.
mutations
analyzed
statistically.
CellMiner
database
drug
prediction
TISCH
single-cell
sequencing
analysis.
We
screened
8
feature
model.
HR
group
had
remarkably
worse
prognosis.
TP53
exhibited
higher
mutation
frequency
group.
analysis
uncovered
remarkable
increase
levels
Macrophages
M0
Tregs
patients.
Drug
sensitivity
demonstrated
expression
IVL
greatly
negatively
linked
with
COLCHICINE.
PTGS2
negative
correlation
Vincristine
sensitivity.
model
can
survival,
status,
potential
drugs
patients,
bringing
new
perspective
individualized
treatment.