PubMed,
Год журнала:
2023,
Номер
13(12), С. 5868 - 5886
Опубликована: Янв. 1, 2023
In
recent
years,
the
role
of
circular
RNAs
(circRNAs)
in
glioma
has
become
increasingly
important.
However,
there
are
still
many
newly
discovered
circRNAs
with
unknown
functions
that
require
further
study.
this
study,
circRNA
sequencing,
qPCR,
MTS,
EdU,
Transwell,
and
other
assays
were
conducted
to
detect
expression
malignant
effects
a
novel
molecule,
circGRIK2,
glioma.
western
blotting,
RIP,
luciferase
reporter
gene
experiments
used
investigate
downstream
molecular
mechanisms
circGRIK2.
Our
study
found
circGRIK2
was
highly
expressed
promoted
cell
viability,
proliferation,
invasion,
migration.
Mechanistically,
acted
as
competitive
sponge
for
miR-1303,
upregulating
HOXA10
exert
its
oncogenic
effects.
Additionally,
RNA-binding
protein
EIF4A3
could
bind
stabilize
leading
high
glioblastoma.
The
discovery
not
only
contributes
better
understanding
biological
but
also
provides
new
target
targeted
therapy.
European Journal of Pharmaceutical Sciences,
Год журнала:
2023,
Номер
191, С. 106586 - 106586
Опубликована: Сен. 19, 2023
Cancer
remains
one
of
the
leading
causes
mortality
worldwide,
presenting
a
significant
healthcare
challenge
owing
to
limited
efficacy
current
treatments.
The
application
nanotechnology
in
cancer
treatment
leverages
unique
optical,
magnetic,
and
electrical
attributes
nanomaterials
engineer
innovative,
targeted
therapies.
Specifically,
manipulating
allows
for
enhanced
drug
loading
efficiency,
improved
bioavailability,
delivery
systems,
reducing
non-specific
cytotoxic
effects
characteristic
conventional
chemotherapies.
Furthermore,
recent
advances
have
demonstrated
encouraging
results
specifically
targeting
CSCs,
key
development
considering
role
these
cells
disease
recurrence
resistance
treatment.
Despite
breakthroughs,
clinical
approval
rates
nano-drugs
not
kept
pace
with
research
advances,
pointing
existing
obstacles
that
must
be
addressed.
In
conclusion,
presents
novel,
powerful
tool
fight
against
cancer,
particularly
elusive
treatment-resistant
CSCs.
This
comprehensive
review
delves
into
intricacies
nanotherapy,
explicitly
stem
cells,
their
markers,
associated
signaling
pathways.
Aging and Disease,
Год журнала:
2024,
Номер
unknown, С. 0 - 0
Опубликована: Янв. 1, 2024
This
comprehensive
review
navigates
the
complex
relationship
between
cellular
aging,
senescence,
and
cancer,
unraveling
determinants
of
fate.
Beginning
with
an
overview
aging's
significance
in
explores
processes,
changes,
molecular
pathways
influencing
senescence.
The
senescence
as
a
dual
mechanism
acting
suppressor
contributor,
focusing
on
its
impact
therapy
response.
highlights
opportunities
for
cancer
therapies
that
target
further
examines
senescence-associated
secretory
phenotype
strategies
to
modulate
aging
influence
tumor
behavior.
Additionally,
mechanisms
escape
cells,
emphasizing
their
prognosis
resistance
therapy.
article
addresses
current
advances,
unexplored
aspects,
future
perspectives
understanding
cancer.
Cancers,
Год журнала:
2024,
Номер
16(8), С. 1557 - 1557
Опубликована: Апрель 19, 2024
On
a
molecular
level,
glioma
is
very
diverse
and
presents
whole
spectrum
of
specific
genetic
epigenetic
alterations.
The
tumors
are
unfortunately
resistant
to
available
therapies
the
survival
rate
low.
explanation
significant
intra-
inter-tumor
heterogeneity
infiltrative
capability
gliomas,
as
well
its
resistance
therapy,
recurrence
aggressive
behavior,
lies
in
small
subset
tumor-initiating
cells
that
behave
like
stem
known
cancer
(GCSCs).
They
responsible
for
tumor
plasticity
influenced
by
drivers.
Additionally,
GCSCs
also
display
greater
migratory
abilities.
A
great
effort
under
way
order
find
ways
eliminate
or
neutralize
GCSCs.
Many
different
treatment
strategies
currently
being
explored,
including
modulation
microenvironment,
posttranscriptional
regulation,
immunotherapy.
Cellular and Molecular Life Sciences,
Год журнала:
2023,
Номер
80(9)
Опубликована: Авг. 29, 2023
We
previously
reported
that
TRPM7
regulates
glioma
cells'
stemness
through
STAT3.
In
addition,
we
demonstrated
FOSL1
is
a
response
gene
for
TRPM7,
and
the
serves
as
an
oncogene
to
promote
proliferation
invasion.In
present
study,
determined
effects
of
on
stem
cell
(GSC)
markers
CD133
ALDH1
by
flow
cytometry,
maintenance
activity
extreme
limiting
dilution
assays
(ELDA).
To
further
gain
insight
into
mechanism
which
activates
transcription
contribute
stemness,
constructed
promoter
its
GAS
mutants
followed
luciferase
reporter
ChIP-qPCR
in
line
patient-derived
xenoline.
examined
GSC
well
immunohistochemistry
staining
(IHC)
brain
tissue
microarray
(TMA)
patients.We
revealed
knockdown
reduces
expression
ALDH1,
required
maintain
cells.
The
experiments
also
showed
mutations
-
328
336
378
386
elements
markedly
reduced
activity.
Constitutively
active
STAT3
increased
while
dominant-negative
decreased
Furthermore,
overexpression
enhanced
silencing
STAT3,
nuclear
lysates
cells
stimulated
constitutively
activated
can
bind
two
elements,
respectively.
deacetylation
at
Lys-116
residue
located
within
DNA
binding
domain
led
increase
transcriptional
found
protein
associated
with
grades
malignant
glioma,
correlates
patients.These
combined
results
induced
activation,
mediated
action
shown
be
important
stemness.
These
indicated
FOSL1,
similar
diagnostic
marker
potential
drug
target
patients.
Acta Neuropathologica Communications,
Год журнала:
2025,
Номер
13(1)
Опубликована: Апрель 30, 2025
Mutations
in
isocitrate
dehydrogenase
(IDH)1/2
are
defining
drivers
of
low-grade
gliomagenesis.
However,
mutant
IDH
alone
is
not
sufficient
for
malignant
transformation,
and
additional
events
required
the
development
glioma.
While
specific
genetic
lesions
have
been
identified
to
contribute
gliomagenesis,
less
known
about
signaling
pathways
involved
acquisition
malignancy.
To
identify
prerequisites
tumorigenesis,
we
modulated
previously
implicated
glioma
initiation
using
a
tractable
vitro
model
system
early
IDH1R132H-dependent
Through
use
chemical
compounds,
targeted
WNT/GSK3,
TGF-β
NOTCH-signaling,
assessing
their
functional,
transcriptional,
translational
impacts.
Expression
LGG-related
marker
L1CAM
was
affected
by
perturbation
all
pathways,
though
only
modulation
WNT/GSK3-signaling
resulted
profound
molecular
including
glioma-associated
genes
programs
regulating
cellular
architecture
cell
replication.
This
accompanied
altered
morphology,
migration
capacity,
enhanced
proliferation.
Transcription
factor
RUNX2
as
potential
downstream
effector,
whose
inhibition
abrogated
Disrupted
WNT/GSK3
gliomagenesis
fundamentally
impacted
fate,
demonstrated
reshaped
transcriptional
landscape,
aberrant
transcription
activity,
extracellular
matrix
restructuring,
proliferation
capacity.
Our
data
suggests
that
GSK3
may
play
central
role
during
warranting
further
investigation.
