Cell Death Discovery,
Journal Year:
2025,
Volume and Issue:
11(1)
Published: Jan. 18, 2025
A
new
type
of
nonapoptotic,
iron-dependent
cell
death
induced
by
lipid
peroxidation
is
known
as
ferroptosis.
Numerous
pathological
processes,
including
inflammation
and
cancer,
have
been
demonstrated
to
be
influenced
changes
in
the
ferroptosis-regulating
network.
Long
non-coding
RNAs
(LncRNAs)
are
a
group
functional
RNA
molecules
that
not
translated
into
proteins,
which
can
regulate
gene
expression
various
manners.
An
increasing
number
studies
shown
lncRNAs
interfere
with
progression
ferroptosis
modulating
ferroptosis-related
genes
directly
or
indirectly.
Despite
evidence
implicating
cancer
inflammation,
on
their
mechanisms
therapeutic
potential
remain
scarce.
We
investigate
lncRNA-mediated
regulation
immunity,
assessing
feasibility
challenges
targets
these
conditions.
Cell Death and Disease,
Journal Year:
2024,
Volume and Issue:
15(5)
Published: May 22, 2024
Abstract
As
a
newly
identified
regulated
cell
death,
ferroptosis
is
metabolically
driven
process
that
relies
on
iron
and
associated
with
polyunsaturated
fatty
acyl
peroxidation,
elevated
levels
of
reactive
oxygen
species
(ROS),
mitochondrial
damage.
This
distinct
death
dysregulated
in
various
cancers;
activating
malignant
cells
increases
cancer
immunotherapy
chemoradiotherapy
responses
across
different
malignancies.
Over
the
last
decade,
accumulating
research
has
provided
evidence
cross-talk
between
non-coding
RNAs
(ncRNAs)
competing
endogenous
RNA
(ceRNA)
networks
highlighted
their
significance
developing
progressing
Aside
from
pharmaceutical
agents
to
regulate
ferroptosis,
recent
studies
have
shed
light
potential
restoring
ferroptosis-related
ceRNA
treatment.
The
present
study
provides
comprehensive
up-to-date
review
significance,
pathways,
role
chemoradiotherapy,
biogenesis,
ferroptosis-regulating
cancers.
insights
can
offer
authorship
state-of-the-art
findings
future
perspectives
regarding
implication
treatment
determining
prognosis
affected
patients.
Cell Death and Disease,
Journal Year:
2024,
Volume and Issue:
15(6)
Published: June 15, 2024
Abstract
Tamoxifen
has
been
the
mainstay
therapy
to
treat
early,
locally
advanced,
and
metastatic
estrogen
receptor-positive
(ER
+
)
breast
cancer,
constituting
around
75%
of
all
cases.
However,
emergence
resistance
is
common,
necessitating
identification
novel
therapeutic
targets.
Here,
we
demonstrated
that
long-noncoding
RNA
LINC00152
confers
tamoxifen
by
blocking
tamoxifen-induced
ferroptosis,
an
iron-mediated
cell
death.
Mechanistically,
inhibiting
reduces
mRNA
stability
phosphodiesterase
4D
(
PDE4D
),
leading
activation
cAMP/PKA/CREB
axis
increased
expression
TRPC1
Ca
2+
channel.
This
causes
cytosolic
overload
generation
reactive
oxygen
species
(ROS)
is,
on
one
hand,
accompanied
downregulation
FTH1,
a
member
iron
sequestration
unit,
thus
increasing
intracellular
Fe
levels;
other
inhibition
peroxidase
activity
upon
reduced
GPX4
xCT
levels,
in
part
cAMP/CREB.
These
ultimately
restore
tamoxifen-dependent
lipid
peroxidation
ferroptotic
death
which
are
reversed
chelating
or
overexpressing
xCT.
Overexpressing
reverses
inhibition-mediated
sensitization
de-activating
cAMP/Ca
/ferroptosis
axis.
Importantly,
high
significantly
correlated
with
PDE4D/low
ferroptosis
worse
survival
multiple
cohorts
tamoxifen-
tamoxifen-containing
endocrine
therapy-treated
ER+
cancer
patients.
Overall,
identified
as
mechanism
via
restoring
destabilizing
PDE4D,
cAMP
ROS
peroxidation.
Our
findings
reveal
its
effectors
actionable
targets
improve
clinical
outcome
refractory
cancer.
Cell Death Discovery,
Journal Year:
2025,
Volume and Issue:
11(1)
Published: Jan. 18, 2025
A
new
type
of
nonapoptotic,
iron-dependent
cell
death
induced
by
lipid
peroxidation
is
known
as
ferroptosis.
Numerous
pathological
processes,
including
inflammation
and
cancer,
have
been
demonstrated
to
be
influenced
changes
in
the
ferroptosis-regulating
network.
Long
non-coding
RNAs
(LncRNAs)
are
a
group
functional
RNA
molecules
that
not
translated
into
proteins,
which
can
regulate
gene
expression
various
manners.
An
increasing
number
studies
shown
lncRNAs
interfere
with
progression
ferroptosis
modulating
ferroptosis-related
genes
directly
or
indirectly.
Despite
evidence
implicating
cancer
inflammation,
on
their
mechanisms
therapeutic
potential
remain
scarce.
We
investigate
lncRNA-mediated
regulation
immunity,
assessing
feasibility
challenges
targets
these
conditions.