Research Square (Research Square),
Journal Year:
2023,
Volume and Issue:
unknown
Published: Dec. 12, 2023
Abstract
Background
Osteosarcoma
(OS)
is
one
of
the
most
common
aggressive
bone
malignancy
tumors
in
adolescents.
With
no
significant
advances
treatment
OS
recent
ten
years,
discovering
new
and
effective
anti-OS
drugs
became
our
top
priority.
Oridonin
has
been
proved
to
mediate
anti-tumor
impact
on
cells,
although
it’s
mechanism
action
not
fully
understood.
Methods
Here,
we
investigated
inhibitory
effect
oridonin
cells
its
underlying
mechanisms.
In
143B
U2OS
oridonin’s
pro-apoptosis
pro-ferroptosis
effects
cell
death,
proliferation,
migration,
iron
accumulation,
mitochondrial
membrane
potential
lipid
peroxidation
production
were
observed.
Western
blot
(WB)
real-time
reverse
transcriptase-polymerase
chain
reaction
(RT-qPCR)
used
detect
expression
levels
apoptosis
ferroptosis-relative
proteins
genes.
Iron
assay
Kit
was
evaluate
relative
Fe
2+
content.
The
detection
kit
ROS
production.
changes
malignant
phenotype
examined
after
treating
with
ferroptosis
inhibitor
ferrostatin-1
(Fer-1).
Results
potently
inhibited
viability
metastasis.
Simultaneously,
suppressed
expressions
BAX,
cl-caspase3,
SLC7A11,
GPX4
FTH1
mRNA,
while
promoting
Bcl-2
ACSL4
143
cells.
Furthermore,
found
that
also
boosted
accumulation
reactive
oxygen
species
(ROS),
encouraged
buildup
,
decreased
but
this
can
be
reversed
by
Fer-1.
Conclusion
trigger
collaboratively
making
it
a
promising
agent
for
therapy.
Nature Communications,
Journal Year:
2024,
Volume and Issue:
15(1)
Published: May 21, 2024
Abstract
Prodrugs
have
been
explored
as
an
alternative
to
conventional
chemotherapy;
however,
their
target
specificity
remains
limited.
The
tumor
microenvironment
harbors
a
range
of
microorganisms
that
potentially
serve
tumor-targeting
vectors
for
delivering
prodrugs.
In
this
study,
we
harness
bacteria-cancer
interactions
native
the
microbiome
achieve
high
prodrug
delivery.
We
identify
oral
commensal
strain
Lactobacillus
plantarum
with
intrinsic
cancer-binding
mechanism
and
engineer
enable
surface
loading
anticancer
prodrugs,
nasopharyngeal
carcinoma
(NPC)
model
cancer.
engineered
commensals
show
specific
binding
NPC
via
OppA-mediated
recognition
heparan
sulfate,
loaded
prodrugs
are
activated
by
tumor-associated
biosignals
release
SN-38,
chemotherapy
compound,
near
NPC.
vitro
experiments
demonstrate
prodrug-loaded
microbes
significantly
increase
potency
SN-38
against
cell
lines,
up
10-fold.
mouse
xenograft
model,
intravenous
injection
L.
leads
bacterial
colonization
in
tumors
67%
inhibition
growth,
enhancing
efficacy
54%.
Heliyon,
Journal Year:
2024,
Volume and Issue:
10(18), P. e37613 - e37613
Published: Sept. 1, 2024
Oxaliplatin
(OXA)-based
therapy
is
effective
in
the
treatment
of
multiple
cancers.
However,
primary
or
acquired
OXA
resistance
remains
an
emerging
challenge
for
its
clinical
application.
Ferroptosis
iron-dependent
mode
cell
death
that
has
been
demonstrated
to
play
essential
role
chemoresistance
many
drugs,
including
OXA.
In
particular,
dysregulation
SLC7A11-GPX4,
one
major
antioxidant
systems
ferroptosis,
was
found
colorectal
cancer
(CRC)
and
hepatocellular
carcinoma
(HCC).
addition,
Nrf2,
upstream
regulator
GPX4
other
factors,
also
involved
CRC
HCC.
Inhibition
SLC7A11-GPX4
Nrf2
by
genetic
deletion
pharmaceutical
inhibition
could
significantly
reverse
resistance.
Long
noncoding
RNA
(lncRNA)
participates
ferroptosis
cells.
Specifically,
LINC01134
promotes
recruitment
promoter
GPX4,
thereby
exerting
transcriptional
regulation
which
eventually
increases
sensitivity
HCC
through
upregulation
ferroptosis.
On
hand,
a
novel
lncRNA
DACT3-AS1
sensitizes
gastric
cells
miR-181a-5p/sirtuin
1(SIRT1)-mediated
Therapies
based
on
combination
enhancers
provide
new
therapeutic
insights
overcome
present
review,
we
current
understanding
ferroptosis-related
resistance,
highlight
pathogenesis
chemoresistance,
summarize
available
therapies
target
enhancing
Cell Death and Disease,
Journal Year:
2025,
Volume and Issue:
16(1)
Published: Jan. 16, 2025
Approximately
80%
of
nasopharyngeal
carcinoma
(NPC)
patients
exhibit
EGFR
overexpression.
The
overexpression
has
been
linked
to
its
potential
role
in
modulating
major
histocompatibility
complex
class
I
(MHC-I)
molecules.
We
discovered
that
EGFR,
operating
a
kinase-independent
manner,
played
stabilizing
the
expression
SLC7A11,
which
subsequently
inhibited
MHC-I
antigen
presentation.
This
mechanism,
turn,
provided
protection
NPC
cells
against
T
cell-mediated
cytotoxicity.
underlying
molecular
processes
revealed
high
and
stable
SLC7A11
hindered
nuclear
entry
GR,
thereby
suppressing
TAP1
transcription
presentation
Additionally,
elevated
led
an
increase
FAF2
triggered
ERAD-dependent
degradation
MHC-I,
resulting
reduction
molecules
on
cell
membrane.
exhibiting
low
expression,
combined
with
scarcity
CD8+
(EGFRhighMHC-IlowCD8few
phenotype),
experienced
considerably
shorter
overall
survival
times
compared
other
situations.
What
is
more,
our
study
demonstrated
sorafenib
had
capability
enhance
process,
facilitating
killing
via
targeting
SLC7A11.
Consequently,
emerges
as
promising
therapeutic
strategy
for
treatment
NPC.
New Journal of Chemistry,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 1, 2025
Ferroptosis
plays
an
extremely
significant
role
in
the
development
of
hepatocellular
carcinoma
(HCC),
and
targeting
tumor
cells
to
induce
ferroptosis
has
emerged
as
a
new
approach
for
treatment
cancer.
Frontiers in Cardiovascular Medicine,
Journal Year:
2025,
Volume and Issue:
12
Published: May 2, 2025
Myocardial
infarction,
as
the
principal
type
of
ischemic
heart
disease,
has
currently
become
focus
research
on
its
prevention
and
treatment
strategies.
From
perspective
myocardial
infarction
pathogenesis,
it
is
urgent
to
impede
progression
this
disease
improve
diagnosis
techniques.
Ferroptosis,
a
form
programmed
cell
death
mechanistically
distinct
from
apoptosis
autophagy,
implicated
throughout
pathogenesis
infarction.
Dysregulation
protein
translation
leads
abnormal
expression,
disruption
cellular
signaling,
dysfunction,
thereby
disturbing
normal
function
exacerbating
progression.
Consequently,
clarifying
mechanism
dysregulation
in
ferroptosis
during
will
enhance
understanding
In
review,
latest
progress
relationship
between
collected.
The
mechanisms
by
which
they
regulate
are
explored,
current
status
role
different
stages
introduced.
These
findings
expected
provide
valuable
insights
for
pathophysiological
precise
treatment.