Cell Death and Disease,
Journal Year:
2024,
Volume and Issue:
15(11)
Published: Nov. 8, 2024
A
hallmark
of
glioma
cells,
particularly
glioblastoma
multiforme
(GBM)
is
their
resistance
to
apoptosis.
Accumulating
evidences
has
demonstrated
that
CARD16,
a
caspase
recruitment
domain
(CARD)
only
protein,
enhances
both
anti-apoptotic
and
tumorigenic
properties.
Nevertheless,
there
limited
understanding
the
expression
functional
role
CARD16
in
glioma.
This
study
seeks
investigate,
through
silico
analysis
clinical
specimens,
as
potential
tumor
promoter
Functional
assays
molecular
studies
revealed
promotes
tumorigenesis
suppresses
apoptosis
cells.
Moreover,
knockdown
FOXO1/TRAIL
axis
GBM
Additionally,
FOXO1
downregulation
cells
restores
proliferation
reduces
Further
investigation
elevated
P21
inhibits
CDK2-mediated
phosphorylation
ubiquitination
CARD16-knockdown
Collectively,
these
findings
suggest
tumor-promoting
via
downregulating
axis,
suppressing
TRAIL-induced
The
gene
presents
significant
for
prognostic
prediction
advances
innovative
apoptotic
therapeutics.
Frontiers in Cell and Developmental Biology,
Journal Year:
2024,
Volume and Issue:
12
Published: March 18, 2024
The
global
challenge
posed
by
cancer,
marked
rising
incidence
and
mortality
rates,
underscores
the
urgency
for
innovative
therapeutic
approaches.
PI3K/Akt
signaling
pathway,
frequently
amplified
in
various
cancers,
is
central
regulating
essential
cellular
processes.
Its
dysregulation,
often
stemming
from
genetic
mutations,
significantly
contributes
to
cancer
initiation,
progression,
resistance
therapy.
Concurrently,
ferroptosis,
a
recently
discovered
form
of
regulated
cell
death
characterized
iron-dependent
processes
lipid
reactive
oxygen
species
buildup,
holds
implications
diseases,
including
cancer.
Exploring
interplay
between
dysregulated
pathway
ferroptosis
unveils
potential
insights
into
molecular
mechanisms
driving
or
inhibiting
ferroptotic
cells.
Evidence
suggests
that
may
sensitize
cells
induction,
offering
promising
strategy
overcome
drug
resistance.
This
review
aims
provide
comprehensive
exploration
this
interplay,
shedding
light
on
disrupting
enhance
as
an
alternative
route
inducing
improving
treatment
outcomes.
Journal for ImmunoTherapy of Cancer,
Journal Year:
2025,
Volume and Issue:
13(2), P. e010192 - e010192
Published: Feb. 1, 2025
Molecular
mimicry
between
commensal
bacterial
antigens
and
tumor-associated
(TAAs)
has
shown
potential
in
enhancing
antitumor
immune
responses.
This
study
leveraged
this
concept
using
antigens,
termed
OncoMimics,
to
induce
TAA-derived
peptide
(TAAp)-specific
cross-reactive
cytotoxic
T
cells
improve
the
efficacy
of
peptide-based
immunotherapies.
The
discovery
OncoMimics
primarily
relied
on
a
bioinformatics
approach
identify
bacteria-derived
sequences
mimicking
TAAps.
Several
(OMP)
candidates
were
selected
silico
based
multiple
key
parameters
assess
their
elicit
ameliorate
responses
against
TAAs.
Selected
OMPs
synthesized
tested
for
affinity
stability
major
histocompatibility
complex
(MHC)
vitro
capacity
OMP-specific/TAAp-specific
CD8+T
cell
human
leukocyte
antigen
(HLA)-A2-humanized
mice,
peripheral
blood
mononuclear
(PBMC)
patients
with
cancer.
demonstrated
superior
HLA-A2
binding
affinities
stabilities
compared
homologous
Vaccination
HLA-A2-humanized
mice
led
expansion
OMP-specific
that
recognize
both
TAAps,
exhibiting
capacities
towards
tumor
resulting
protection
prophylactic
setting.
Using
PBMCs
from
HLA-A2+healthy
donors,
we
confirmed
ability
potent
CD8+
T-cell
Interestingly,
observed
high
prevalence
across
donors.
Cytotoxicity
assays
revealed
OMP-stimulated
specifically
targeted
killed
loaded
or
Preliminary
data
an
ongoing
clinical
trial
(NCT04116658)
support
these
findings,
indicating
robust
patients.
Initial
immunomonitoring
sustained
over
time,
maintaining
polyfunctional,
memory
phenotype,
which
is
critical
effective
activity
long-term
surveillance.
These
findings
suggest
leveraging
naturally
occurring
commensal-derived
through
could
significantly
remodel
landscape,
offering
guidance
promising
strategy
cancer
Frontiers in Cell and Developmental Biology,
Journal Year:
2024,
Volume and Issue:
12
Published: Oct. 29, 2024
CHAC1,
an
essential
regulator
of
oxidative
stress
and
ferroptosis,
is
increasingly
recognized
for
its
significant
roles
in
these
cellular
processes
impact
on
various
human
diseases
cancers.
This
review
aims
to
provide
a
comprehensive
overview
CHAC1's
molecular
functions,
regulatory
mechanisms,
effects
different
pathological
contexts.
Specifically,
the
study
objectives
are
elucidate
biochemical
pathways
involving
explore
network,
discuss
implications
disease
progression
potential
therapeutic
strategies.
As
γ-glutamyl
cyclotransferase,
CHAC1
degrades
glutathione,
affecting
calcium
signaling
mitochondrial
function.
Its
regulation
involves
transcription
factors
like
ATF4
ATF3,
which
control
mRNA
expression.
crucial
maintaining
redox
balance
regulating
cell
death
cancer.
elevated
levels
associated
with
poor
prognosis
many
cancers,
indicating
as
biomarker
target.
Additionally,
influences
non-cancerous
such
neurodegenerative
cardiovascular
disorders.
Therapeutically,
targeting
could
increase
cancer
sensitivity
aiding
overcoming
resistance
standard
treatments.
compiles
current
knowledge
recent
discoveries,
emphasizing
vital
role
diagnostic
applications.
Clinics,
Journal Year:
2024,
Volume and Issue:
79, P. 100350 - 100350
Published: Jan. 1, 2024
The
present
study
aimed
to
investigate
FOXO3a
deregulation
in
Uterine
Smooth
Muscle
Tumors
(USMT)
and
its
potential
association
with
cancer
development
prognosis.
authors
analyzed
gene
protein
expression
profiles
of
56
uterine
Leiomyosarcomas
(LMS),
119
leiomyomas
(comprising
conventional
unusual
leiomyomas),
20
Myometrium
(MM)
samples.
used
techniques
such
as
Immunohistochemistry
(IHC),
FISH/CISH,
qRT-PCR
for
the
analyses.
Additionally,
conducted
an
in-silico
analysis
understand
interaction
network
involving
correlated
genes.
This
investigation
revealed
distinct
patterns
protein,
including
both
normal
phosphorylated
forms.
Expression
levels
were
notably
elevated
LMS,
Unusual
Leiomyomas
(ULM)
compared
(LM)
upregulation
was
significantly
associated
metastasis
Overall
Survival
(OS)
LMS
patients.
Intriguingly,
did
not
seem
be
influenced
by
EGF/HER-2
signaling,
there
minimal
EGF
VEGF
detected,
HER-2
EGFR
negative
In
examination
miRNAs,
observed
miR-96-5p
miR-155-5p,
which
are
known
regulators
FOXO3a,
Conversely,
tumor
suppressor
miR-let7c-5p
downregulated.
summary,
outcomes
suggest
that
imbalance
within
might
arise
from
phosphorylation
miRNA
activity.
could
emerge
a
promising
therapeutic
target
individuals
(ULM
LMS),
offering
novel
directions
treatment
strategies.