Cancer Drug Resistance,
Journal Year:
2024,
Volume and Issue:
unknown
Published: May 7, 2024
Glioma
accounts
for
81%
of
all
cancers
the
nervous
system
and
presents
one
most
drug-resistant
malignancies,
resulting
in
a
relatively
high
mortality
rate.
Despite
extensive
efforts,
complete
treatment
options
glioma
remain
elusive.
The
effect
isocucurbitacin
B
(isocuB),
natural
compound
extracted
from
melon
pedicels,
on
has
not
been
investigated.
This
study
aims
to
investigate
inhibitory
isocuB
elucidate
its
underlying
mechanisms,
with
objective
developing
it
as
potential
therapeutic
agent
glioma.
Frontiers in Pharmacology,
Journal Year:
2025,
Volume and Issue:
15
Published: Jan. 14, 2025
Hydroxysafflor
yellow
A
(HSYA),
a
natural
pigment
with
chalcone
structure
extracted
from
Carthamus
tinctorius
L.
(Safflower),
has
been
widely
proven
to
have
good
efficacy
on
cardiovascular
diseases,
atherosclerosis,
cancer,
and
diabetes.
However,
no
study
reported
the
anticancer
mechanisms
of
principal
bioactive
compound
in
safflower.
This
review
discusses
recent
developments
physicochemical
properties
sources,
pharmacological
effects
mechanisms,
pharmacokinetic
progress,
safety
HSYA,
focusing
involvement
HSYA
regulation
related
pathways
apoptosis,
autophagy,
tumor
immune
microenvironment
variety
cancers.
can
serve
as
theoretical
basis
for
further
research
development
insights
into
signaling
pathways.
Gliomas
are
devastating,
incurable
malignant
tumors
with
high
recurrence
rates
and
frequent
treatment
failures
due
to
their
resistance
complete
surgical
resection.
We
found
that
isocucurbitacin
B
significantly
inhibited
the
proliferation,
invasion,
migration,
epithelial-mesenchymal
transition
(EMT)
of
glioma
cells
by
downregulating
expression
MMP2,
N-cadherin,
vimentin.
Moreover,
reduced
CDK1
cyclin
A2,
resulting
in
G2/M
phase
arrest
U251
cells.
Isocucurbitacin
induced
apoptosis
increasing
cleaved
caspase-3
BAX/BCL-2
ratio
levels.
Simultaneously,
promoted
anoikis
decreasing
caveolin
1,
focal
adhesion
kinase
phosphorylation,
tropomyosin
receptor
The
cellular
thermal
shift
assay
further
confirmed
direct
binding
1.
Additionally,
activated
BKCa
calcium
channel
cells,
leading
increased
intracellular
Ca2+
levels
decreased
pH.
In
vivo,
tumor
growth
zebrafish
patient-derived
xenograft
situ
mouse
models.
Our
results
suggest
a
potential
link
between
ion
channels
highlight
role
cholesterol
metabolism
regulation.
promising
B's
as
therapeutic
agent
gliomas.
Frontiers in Immunology,
Journal Year:
2025,
Volume and Issue:
16
Published: April 14, 2025
Background
Recent
studies
have
highlighted
the
importance
of
cross-talk
along
gut-brain
axis
in
regulating
inflammatory
nociception,
responses,
and
immune
homeostasis.
The
gut
microbiota,
particularly
its
bacterial
composition,
plays
a
crucial
role
development
function
system.
Moreover,
metabolites
produced
by
microbiota
can
significantly
impact
both
systemic
responses
central
nervous
system
(CNS)
immunity.
Sodium
butyrate
is
key
metabolite
and,
as
histone
deacetylase
inhibitor,
enhance
anti-tumor
immunity
cytotoxic
CD8
+
T
cells.
However,
it
remains
unclear
whether
sodium
treatment
efficacy
PD-1
blockade
glioma
therapy.
In
this
research,
effect
underlying
mechanism
combination
anti-mouse
mAb
on
has
been
investigated.
Methods
RNA-seq
assay
cell
biomedical
databases,
including
ONCOMINE,
GEPIA
TCGA
were
incorporated.
Subsequently,
inhibitory
cells
related
mechanisms
assessed
through
Counting
Kit-8
(CCK-8),
Flow
Cytometry,
Western
blot
(WB),
reverse
transcription-quantitative
polymerase
chain
reaction
(RT-qPCR),
other
vitro
experiments.
,
an
orthotopic
mouse
model
was
established.
MRI
imaging,
Immunohistochemistry,
Immune
flow
cytometry
used
to
investigate
therapeutic
effects
combined
inhibitor
glioma-bearing
mice.
Results
We
discovered
that
deacetylation-associated
gene
expression
increased
patients
affects
patient
survival
time.
we
found
promoted
apoptosis,
disrupted
cycle,
inhibited
tumor
growth.
Additionally,
may
upregulate
PD-L1
modulating
PI3K/AKT
pathway.
experimental
results
demonstrated
therapy
reduced
volume
prolonged
murine
model.
led
increase
proportion
probiotic
bacteria
resulting
elevated
levels
antitumor
decrease
affect
function.
Cell Death Discovery,
Journal Year:
2025,
Volume and Issue:
11(1)
Published: May 21, 2025
Abstract
Glioblastomas
(GBMs)
are
aggressive
brain
tumors
and
challenging
cancers
for
diagnosis
treatment.
Therapeutic
options
include
surgery
followed
by
chemotherapy
with
the
DNA
alkylator
temozolomide
(TMZ)
radiotherapy.
However,
patient's
prognosis
remains
poor
due
to
tumor
heterogeneity,
cell
infiltration
intrinsic
or
acquired
resistance
therapy.
Understanding
mechanisms
together
identifying
new
biomarkers
crucial
developing
novel
therapeutic
strategies.
MiRNAs
play
an
important
role
in
biology
of
gliomas,
they
modulate
tumorigenesis
therapy
response.
We
recently
identified
diagnostic/prognostic
miR-1-3p,
miR-26a-1-3p
miR-487b-3p
signature
that
displays
oncosuppressive
on
several
glioma
biological
functions.
In
this
study,
we
investigated
effects
potential
three-miRNA
as
a
regulator
response
TMZ.
found
ectopic
expression
miRNA
patient-derived
GBM
neurospheres
treated
TMZ
impaired
proliferation
viability
necroptosis
induction.
Moreover,
WT1
FOXA1,
two
transcription
factors
specifically
involved
resistance,
direct
targets
signature.
Of
note,
repression
elicited
signature,
caused
downregulation
Androgen
Receptor
(AR)
expression,
impairment
tumor-spheroid
formation
reversed
cancer
stemness.
These
results
were
recapitulated
using
AR
inhibitor
enzalutamide,
confirming
involvement
pathway.
Our
data
indicate
miR-1-3p/miR-26a-1-3p/miR-487b-3p
which
has
impact
treatment
stemness,
may
pave
way
miRNA-based
complementary
therapies
patients.
Biomedicines,
Journal Year:
2024,
Volume and Issue:
12(7), P. 1546 - 1546
Published: July 11, 2024
In
addition
to
necrosis
and
apoptosis,
the
two
forms
of
cell
death
that
have
been
known
for
many
decades,
other
non-apoptotic
discovered,
which
also
play
a
role
in
tumors.
Starting
with
description
autophagy
more
than
60
years
ago,
newer
become
important
biology
tumors,
such
as
ferroptosis,
pyroptosis,
necroptosis,
paraptosis.
this
review,
all
oncologically
relevant
programmed
are
presented,
starting
their
first
descriptions,
molecular
characteristics,
interactions
physiology
pathophysiology.
Based
on
these
current
state
knowledge
about
alterations
gliomas
will
be
presented.
addition,
efforts
therapeutically
influence
components
discussed.
Although
research
into
exact
is
still
at
rather
early
stage,
our
review
clarifies
show
significant
insight
understanding
them
has
already
gained.
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: Dec. 19, 2024
A
comprehensive
understanding
of
tumor
heterogeneity,
microenvironment
and
the
mechanisms
drug
resistance
is
fundamental
to
advancing
breast
cancer
research.
While
single-cell
RNA
sequencing
has
resolved
issue
"temporal
dynamic
expression"
genes
at
level,
lack
spatial
information
still
prevents
us
from
gaining
a
cancer.
The
introduction
application
transcriptomics
addresses
this
limitation.
As
annual
technical
method
2020,
preserves
location
tissues
resolves
RNA-seq
data
help
localize
differentiate
active
expression
functional
within
specific
tissue
region,
enabling
study
attributes
gene
locations
cellular
environments.
In
context
cancer,
can
assist
in
identification
novel
subtypes
spatially
discriminative
features
that
show
promise
for
individualized
precise
treatment.
This
article
summarized
key
approaches,
recent
advances
its
applications
discusses
limitations
current
methods
prospects
future
development,
with
view
technology
clinical
practice.
Frontiers in Pharmacology,
Journal Year:
2024,
Volume and Issue:
15
Published: Oct. 22, 2024
Introduction
Breast
cancer
is
the
most
common
worldwide,
leading
cause
of
death
in
women,
and
fifth
death.
Triple
negative
breast
(TNBC),
with
high
metastasis
mortality
rates,
challenging
subtype
treatment.
There
an
urgent
need
to
develop
anti-TNBC
drugs
significant
efficacy,
low
side
effects
good
availability.
In
early
drug
screening,
blestriarene
C
was
found
have
inhibitory
on
TNBC
cells.
this
article,
we
further
explore
mechanisms
associated
for
cancer.
Methods
take
approach
network
pharmacology
combined
vivo
vitro
experiments.
Network
analysis
used
predict
active
components
Baiji,
investigate
hub
targets
related
BC
The
mechanism
evaluated
by
CCK-8
assay,
cell
apoptosis
cycle
assays,
wound
healing
WB
molecular
docking
analysis.
inhibition
effect
test
subcutaneous
tumor
models
established
mice.
Results
Through
experiments,
screened
out
as
main
ingredient,
that
could
inhibit
Ras/ERK/c-Fos
signaling
pathway
while
downregulating
expression
HSP90AA1
upregulating
PTGS2,
thereby
promoting
apoptosis,
causing
S-phase
arrest,
inhibiting
proliferation
migration
BT549
results
illustrated
inhibited
growth
tumors
has
a
safety
profile.
By
integrating
study
demonstrated
cells
pathway,
arrest.
Discussion
This
provides
new
evidence
use
novel
