Ecotoxicology and Environmental Safety,
Journal Year:
2024,
Volume and Issue:
273, P. 116098 - 116098
Published: Feb. 17, 2024
Plastic
waste
accumulation
and
its
degradation
into
microplastics
(MPs)
nanoplastics
(NPs)
pose
environmental
concerns.
Previous
studies
have
indicated
that
polystyrene
(PS)-MPs
harm
living
animals.
Extracellular
vesicles
(EVs)
are
associated
with
metabolic
reprogramming
mitochondrial
dysfunction
in
various
kidney
diseases.
In
this
article,
we
evaluated
how
PS-MPs
affected
tubular
cells
fibroblasts.
The
results
demonstrated
increased
EV
production
human
caused
endoplasmic
reticulum
(ER)
stress-related
proteins
without
inducing
inflammation-related
cells.
uptake
of
incubation
the
conditioned
medium
induced
reactive
oxygen
species
(ROS)
ER
fibroblast
treated
also
expression
fibrosis-related
proteins.
Our
findings
suggested
EV-related
markers
via
Beclin
1
after
PS-MP
treatment.
addition,
ROS
vitro
vivo.
We
found
altered
urine,
CD63
was
vivo
conclusion,
PS-MP-induced
EVs
lead
to
proteins,
Cancer Letters,
Journal Year:
2023,
Volume and Issue:
581, P. 216508 - 216508
Published: Nov. 28, 2023
Among
patients
with
triple-negative
breast
cancer
(TNBC),
distant
metastasis
is
the
leading
cause
of
death.
Our
previous
studies
have
shown
that
TNBC
progression
greatly
facilitated
by
circKIF4A,
but
uncertainty
remains
regarding
its
role
in
brain
and
molecular
mechanism.
In
this
study,
we
found
notable
upregulation
circKIF4A
cell
lines
metastases.
Inhibition
impaired
ability
to
proliferate,
migrate,
metastasis.
Luciferase
reporter
assays
confirmed
competed
for
binding
miR-637
STAT3
3’
UTR.
Western
blot
analysis
revealed
inhibition
decreased
p62
expression,
while
increased
LC3B-II/LC3B–I
ratio
expression
Beclin,
indicating
downregulation
induced
autophagy
competing
miR-637.
By
employing
a
competitive
endogenous
RNA
(ceRNA)
mechanism,
circKIF4A-miR-637-STAT3
axis
coordinates
TNBC.
can
therefore
be
used
as
prognostic
biomarker
therapeutic
target.
Autophagy,
Journal Year:
2024,
Volume and Issue:
20(6), P. 1213 - 1246
Published: March 6, 2024
Macroautophagy/autophagy
is
a
complex
degradation
process
with
dual
role
in
cell
death
that
influenced
by
the
types
are
involved
and
stressors
they
exposed
to.
Ferroptosis
an
iron-dependent
oxidative
form
of
characterized
unrestricted
lipid
peroxidation
context
heterogeneous
plastic
mechanisms.
Recent
studies
have
shed
light
on
involvement
specific
autophagy
(e.g.
ferritinophagy,
lipophagy,
clockophagy)
initiating
or
executing
ferroptotic
through
selective
anti-injury
proteins
organelles.
Conversely,
other
forms
reticulophagy
lysophagy)
enhance
cellular
defense
against
damage.
Dysregulated
autophagy-dependent
ferroptosis
has
implications
for
diverse
range
pathological
conditions.
This
review
aims
to
present
updated
definition
ferroptosis,
discuss
influential
substrates
receptors,
outline
experimental
methods,
propose
guidelines
interpreting
results.
Cell Death Discovery,
Journal Year:
2024,
Volume and Issue:
10(1)
Published: March 13, 2024
Abstract
Ferroptosis
is
an
iron
ion-dependent,
regulatory
cell
death
modality
driven
by
intracellular
lipid
peroxidation
that
plays
a
key
role
in
the
development
of
HCC.
Studies
have
shown
various
clinical
agents
(e.g.,
sorafenib)
ferroptosis
inducer-like
effects
and
can
exert
therapeutic
modulating
different
factors
pathway.
This
implies
targeting
tumor
may
be
very
promising
strategy
for
therapy.
In
this
paper,
we
summarize
prerequisites
defense
systems
occurrence
targets
drug-mediated
action
HCC,
differences
connections
between
other
programmed
deaths.
We
aim
to
theoretical
basis,
classical
inducers
research
progress
HCC
cells,
clued
treatment
regulating
network.
Further
investigation
specific
mechanisms
hepatocellular
carcinoma
interventions
at
stages
will
help
us
deepen
our
understanding
carcinoma,
with
view
providing
new
more
precise
preventive
as
well
measures
patients.
NAR Cancer,
Journal Year:
2024,
Volume and Issue:
6(2)
Published: April 8, 2024
Abstract
The
dysregulation
of
ribosome
biogenesis
is
a
hallmark
cancer,
facilitating
the
adaptation
to
altered
translational
demands
essential
for
various
aspects
tumor
progression.
This
review
explores
intricate
interplay
between
and
cancer
development,
highlighting
dynamic
regulation
orchestrated
by
key
oncogenic
signaling
pathways.
Recent
studies
reveal
multifaceted
roles
ribosomes,
extending
beyond
protein
factories
include
regulatory
functions
in
mRNA
translation.
Dysregulated
not
only
hampers
precise
control
global
production
proliferation
but
also
influences
processes
such
as
maintenance
stem
cell-like
properties
epithelial-mesenchymal
transition,
contributing
Interference
with
biogenesis,
notably
through
RNA
Pol
I
inhibition,
elicits
stress
response
marked
nucleolar
integrity
loss,
subsequent
G1-cell
cycle
arrest
or
cell
death.
These
findings
suggest
that
cells
may
rely
on
heightened
transcription,
rendering
ribosomal
synthesis
potential
therapeutic
vulnerability.
further
targeting
vulnerabilities
promising
strategy
disrupt
production,
presenting
opportunities
treatment.
Cancer Letters,
Journal Year:
2024,
Volume and Issue:
597, P. 217076 - 217076
Published: June 19, 2024
Understanding
of
the
metabolic
reprogramming
has
revolutionized
our
insights
into
tumor
progression
and
potential
treatment.
This
review
concentrates
on
aberrant
pathways
in
cancer
cells
within
microenvironment
(TME).
Cancer
differ
from
normal
their
processing
glucose,
amino
acids,
lipids
order
to
adapt
heightened
biosynthetic
energy
needs.
These
shifts,
which
crucially
alter
lactic
acid,
acid
lipid
metabolism,
affect
not
only
cell
proliferation
but
also
TME
dynamics.
explores
various
immune
TME.
From
a
therapeutic
standpoint,
targeting
these
alterations
represents
novel
treatment
strategy.
discusses
approaches
regulation
metabolism
different
nutrients
influencing
enhance
response.
In
summary,
this
summarizes
its
as
target
for
innovative
strategies,
offering
fresh
perspectives
