Frontiers in Pharmacology,
Journal Year:
2022,
Volume and Issue:
13
Published: June 30, 2022
Ferroptosis
is
an
iron-dependent
regulated
form
of
cell
death
caused
by
excessive
lipid
peroxidation.
This
differed
from
known
forms
in
morphological
and
biochemical
features
such
as
apoptosis,
necrosis,
autophagy.
Cancer
cells
require
higher
levels
iron
to
survive,
which
makes
them
highly
susceptible
ferroptosis.
Therefore,
it
was
found
be
closely
related
the
progression,
treatment
response,
metastasis
various
cancer
types.
Numerous
studies
have
that
ferroptosis
pathway
drug
resistance
cancer.
Some
reduce
their
susceptibility
downregulating
pathway,
resulting
anticancer
therapy.
Induction
restores
sensitivity
drug-resistant
standard
treatments.
are
resistant
conventional
therapies
or
a
high
propensity
metastasize
might
particularly
biological
processes
cellular
components,
epithelial–mesenchymal
transition
(EMT)
noncoding
RNAs,
can
influence
regulating
targeting
may
help
suppress
metastasis.
Those
progresses
revealed
importance
cancer,
In
order
provide
detailed
molecular
mechanisms
therapy
strategies
overcome
these
barriers
not
fully
understood,
we
described
key
its
interaction
with
signaling
pathways
Furthermore,
summarized
for
reversing
targeted
therapy,
chemotherapy,
radiotherapy,
immunotherapy
inhibiting
modulating
Understanding
comprehensive
regulatory
new
insights
enhance
efficacy
drugs,
resistance,
inhibit
Cell Death and Disease,
Journal Year:
2023,
Volume and Issue:
14(1)
Published: Jan. 31, 2023
Abstract
Recent
research
has
shown
that
ferroptosis,
the
iron-dependent
accumulation
of
lipid
peroxides
leads
to
cell
death,
suppresses
cancer
metastasis.
However,
role
ferroptosis
in
prostate
metastasis
not
been
completely
elucidated.
In
current
study,
we
identified
essential
serum/glucocorticoid
regulated
kinase
2
(SGK2)
promoting
by
inhibiting
ferroptosis.
We
found
expression
SGK2
was
higher
metastatic
and
predicted
poor
clinical
outcomes.
knockdown
inhibited
capacity
cells
vivo
vitro,
while
overexpression
facilitated
phosphorylating
Thr-24
Ser-319
sites
forkhead
box
O1
(FOXO1).
This
process
induced
translocation
FOXO1
from
nucleus
cytoplasm,
relieving
inhibitory
effect
on
glutathione
peroxidase
4
(GPX4).
These
findings
delineated
a
novel
regulation
metastasis,
identifying
new
key
pathway
driving
potentially
providing
treatment
strategies
for
cancer.
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(2), P. 910 - 910
Published: Jan. 4, 2023
Prostate
cancer
(PCa)
is
the
most
common
male
malignancy
and
fifth
leading
cause
of
death
in
men
worldwide.
cells
are
characterized
by
a
hybrid
glycolytic/oxidative
phosphorylation
phenotype
determined
androgen
receptor
signaling.
An
increased
lipogenesis
cholesterogenesis
have
been
described
PCa
cells.
Many
studies
shown
that
enzymes
involved
these
pathways
overexpressed
PCa.
Glutamine
becomes
an
essential
amino
acid
for
cells,
its
metabolism
thought
to
become
attractive
therapeutic
target.
A
crosstalk
between
stromal
occurs
tumor
microenvironment
because
release
different
cytokines
growth
factors
due
changes
extracellular
matrix.
deeper
insight
into
metabolic
may
be
obtained
multi-omic
approach
integrating
genomics,
transcriptomics,
metabolomics,
lipidomics,
radiomics
data.
