The Journal of Gene Medicine,
Journal Year:
2024,
Volume and Issue:
26(7)
Published: July 1, 2024
Abstract
Background
Hepatocellular
carcinoma
(HCC)
is
a
malignant
tumor
with
significant
variability
in
prognosis
among
patients.
Ras‐related
C3
botulinum
toxin
substrate
1
(RAC1)
key
focus
the
area
of
cancer
research.
However,
molecular
mechanisms
RAC1
HCC
remain
incompletely
elucidated.
Materials
and
methods
In
this
study,
bioinformatics
analysis
was
used,
public
databases
were
used
to
obtain
information
about
cases.
The
samples
categorized
into
two
groups
high
low
expression
based
on
level
gene.
limma
package
calculate
differentially
expressed
genes
between
groups,
univariate
Cox
regression
screen
prognostic
related
factors.
Consensus
clustering
performed
using
ConsensusClusterPlus
identify
subtypes
Immune
cell
infiltration
ESTIMATE
scores
assessed
single
sample
gene
set
enrichment
algorithms.
sensitivity
different
isoforms
chemotherapeutic
agents
predicted
by
oncoPredict
package.
Finally,
we
also
function
experiments
validate
biological
role
vitro
.
Initially,
classified
patients
levels
identified
195
up‐regulated
107
down‐regulated
genes.
Through
analysis,
screened
out
169
prognosis‐related
Furthermore,
subtypes.
Subsequently,
Kaplan–Meier
survival
curves
showed
that
there
difference
Further
indicated
substantial
differences
TIDE
Moreover,
these
exhibited
varying
chemotherapy
drugs,
as
evidenced
IC
50
values.
addition,
found
silence
could
effectively
inhibit
migration
invasion
cells
Conclusion
This
study
sheds
light
intricacies
identifies
patient
populations
may
benefit
from
immunotherapeutic
interventions,
potential
implications
for
tailored
treatment
strategies.
Circulation,
Journal Year:
2024,
Volume and Issue:
149(24), P. 1903 - 1920
Published: Feb. 15, 2024
S-Nitrosylation
(SNO),
a
prototypic
redox-based
posttranslational
modification,
is
involved
in
cardiovascular
disease.
Aortic
aneurysm
and
dissection
are
high-risk
diseases
without
an
effective
cure.
The
aim
of
this
study
was
to
determine
the
role
SNO
Septin2
macrophages
aortic
dissection.
Journal of Biomolecular Structure and Dynamics,
Journal Year:
2022,
Volume and Issue:
41(15), P. 7511 - 7533
Published: Sept. 12, 2022
Honokiol
(HNK)
is
a
natural
polyphenolic
compound
extracted
from
the
bark
and
leaves
of
Magnolia
grandiflora.
It
has
been
traditionally
used
as
medicinal
to
treat
inflammatory
diseases.
HNK
possesses
numerous
health
benefits
with
minimal
level
toxicity.
can
cross
blood-brain
barrier
blood-cerebrospinal
fluid,
thus
having
significant
bioavailability
in
neurological
tissues.
promising
bioactive
neuroprotective,
antimicrobial,
anti-tumorigenic,
anti-spasmodic,
antidepressant,
analgesic,
antithrombotic
features
.
prevent
growth
several
cancer
types
haematological
malignancies.
Recent
studies
suggested
its
role
COVID-19
therapy.
binds
effectively
molecular
targets,
including
apoptotic
factors,
chemokines,
transcription
cell
surface
adhesion
molecules,
kinases.
excellent
pharmacological
wide
range
chemotherapeutic
effects,
thus,
researchers
have
increased
interest
improving
therapeutic
implications
clinic
novel
agent.
This
review
focused
on
HNK,
highlighting
clinical
underlying
mechanism
action.Communicated
by
Ramaswamy
H.
Sarma
Cell Death and Disease,
Journal Year:
2024,
Volume and Issue:
15(2)
Published: Feb. 20, 2024
Mitochondrial
transfer
plays
an
important
role
in
various
diseases,
and
many
mitochondrial
biological
functions
can
be
regulated
by
HMGB1.
To
explore
the
of
hepatocellular
carcinoma
(HCC)
its
relationship
with
HMGB1,
field
emission
scanning
electron
microscopy,
immunofluorescence,
flow
cytometry
were
used
to
detect
between
HCC
cells.
We
found
that
cells
was
confirmed
using
tunnel
nanotubes
(TNTs).
The
mitochondria
from
highly
invasive
less
could
enhance
migration
invasion
ability
latter.
hypoxic
conditions
increased
Then
mechanism
identified
co-immunoprecipitation,
luciferase
reporter
assay,
chromatin
immunoprecipitation.
RHOT1,
a
transport
protein,
promoted
metastasis
during
this
process.
Under
hypoxia,
HMGB1
further
RHOT1
expression
increasing
NFYA
NFYC
subunits
NF-Y
complex.
RAC1,
protein
associated
TNTs
formation,
development.
Besides,
RAC1
aggregation
cell
membrane
under
hypoxia.
Finally,
changes
significance
related
molecules
clinical
samples
analyzed
bioinformatics
tissue
microarray
analyses.
patients
high
or
exhibited
relatively
shorter
overall
survival
period.
In
conclusion,
conditions,
formation-related
RAC1.
Life Sciences,
Journal Year:
2024,
Volume and Issue:
342, P. 122510 - 122510
Published: Feb. 20, 2024
Rac1
is
a
member
of
the
Rho
GTPase
family
which
plays
major
roles
in
cell
mobility,
polarity
and
migration,
as
fundamental
regulator
actin
cytoskeleton.
Signal
transduction
by
occurs
through
interaction
with
multiple
effector
proteins,
its
activity
regulated
guanine
nucleotide
exchange
factors
(GEFs)
GTPase-activating
proteins
(GAPs).
The
small
protein
mainly
anchored
to
inner
side
plasma
membrane
but
it
can
be
found
endocellular
compartments,
notably
endosomes
nuclei.
localizes
also
into
mitochondria
where
contributes
regulation
mitochondrial
dynamics,
including
both
mitobiogenesis
mitophagy,
addition
signaling
processes
via
different
partners,
such
proapoptotic
Bcl-2
chaperone
sigma-1
receptor
(σ-1R).
form
(mtRac1)
has
been
understudied
thus
far,
essential
nuclear
or
forms,
implication
oxidative
stress
DNA
damages.
subject
diverse
post-translational
modifications,
geranylgeranylation
importantly
import
anchorage
membranes.
In
addition,
translocation
other
p53.
localization
functions
are
discussed
here,
context
human
diseases
cancers.
Inhibitors
have
identified
(NSC-23766,
EHT-1864)
some
being
developed
for
treatment
cancer
(MBQ-167)
central
nervous
system
(JK-50561).
Their
effects
on
mtRac1
warrant
further
investigations.
An
overview
provided
here.
Ecotoxicology and Environmental Safety,
Journal Year:
2025,
Volume and Issue:
289, P. 117641 - 117641
Published: Jan. 1, 2025
Sodium
arsenite
(NaAsO2),
the
most
common
form
of
inorganic
arsenic
prevalent
in
environment,
has
been
closely
linked
to
islet
β-cell
dysfunction,
a
critical
pathological
hallmark
type
2
diabetes
(T2D).
Even
though
apoptosis
plays
pivotal
role
arsenic-induced
explicit
underlying
mechanisms
remain
elusive.
Here,
we
have
identified
that
SET-Rac1
signaling
pathway
is
instrumental
and
dysfunction
β-cells
induced
by
NaAsO2.
During
NaAsO2-induced
our
observations
indicated
downregulation
SET
(almost
0.5-fold)
upregulation
Rac1
(0.5-fold).
Notably,
overexpression
or
inhibition
substantially
mitigated
ameliorated
impaired
insulin
secretion
(increased
from
0.1
ng/ml
0.2
ng/ml)
caused
NaAsO2
exposure.
In
addition,
detected
cytoskeletal
disorganization
following
treatment,
characterized
elevated
Cofilin-1
protein
expression
(approximately
2.5-fold)
disrupted
cytoskeleton
arrangement.
Significantly,
deletion
rectified
abnormalities,
as
evidenced
reduced
enhanced
F-actin
fluorescence.
Our
research
delineates
triggers
functional
impairment
through
rearrangement
mediated
pathway.
This
discovery
could
provide
novel
insights
into
therapeutic
strategies
for
T2D
provoked
environmental
toxicants.
Biomarker Research,
Journal Year:
2025,
Volume and Issue:
13(1)
Published: Feb. 26, 2025
Abstract
The
battle
against
cancer
has
evolved
over
centuries,
from
the
early
stages
of
surgical
resection
to
contemporary
treatments
including
chemotherapy,
radiation,
targeted
therapies,
and
immunotherapies.
Despite
significant
advances
in
treatment
recent
decades,
these
therapies
remain
limited
by
various
challenges.
Immune
checkpoint
inhibitors
(ICIs),
a
cornerstone
tumor
immunotherapy,
have
emerged
as
one
most
promising
advancements
treatment.
Although
ICIs,
such
CTLA-4
PD-1/PD-L1
inhibitors,
demonstrated
clinical
efficacy,
their
therapeutic
impact
remains
suboptimal
due
patient-specific
variability
immune
resistance.
Cell
death
is
fundamental
process
for
maintaining
tissue
homeostasis
function.
Recent
research
highlights
that
combination
induced
regulatory
cell
(RCD)
ICIs
can
substantially
enhance
anti-tumor
responses
across
multiple
types.
In
cells
exhibiting
high
levels
recombinant
solute
carrier
family
7
member
11
(SLC7A11)
protein,
glucose
deprivation
triggers
programmed
(PCD)
pathway
characterized
disulfide
bond
formation
REDOX
(reduction-oxidation)
reactions,
termed
“disulfidptosis.”
Studies
suggest
disulfidptosis
plays
critical
role
efficacy
SLC7A11
cancers.
Therefore,
investigate
potential
synergy
between
this
study
will
explore
mechanisms
both
processes
progression,
with
goal
enhancing
response
targeting
intracellular
pathway.
