Cells,
Journal Year:
2020,
Volume and Issue:
9(12), P. 2709 - 2709
Published: Dec. 17, 2020
The
treatment
of
tumors
requires
the
induction
cell
death.
Radiotherapy,
chemotherapy,
and
immunotherapy
are
administered
to
kill
cancer
cells;
however,
some
cells
resistant
these
therapies.
Therefore,
effective
treatments
require
various
strategies
for
Regulated
death
(RCD)
is
systematically
controlled
by
intracellular
signaling
proteins.
Apoptosis
autophagy
types
RCD
that
morphologically
different
from
necrosis,
while
necroptosis,
pyroptosis,
ferroptosis
similar
necrosis.
Unlike
regulated
necrotic
(RNCD)
caused
disruption
plasma
membrane
under
control
specific
proteins
induces
tissue
inflammation.
Various
RNCD,
such
as
ferroptosis,
have
been
used
therapeutic
against
tumor
types.
In
this
review,
mechanisms
described
in
detail,
a
potential
strategy
increase
anticancer
effects
on
apoptosis-
or
autophagy-resistant
through
RNCD
suggested.
Nutrients,
Journal Year:
2021,
Volume and Issue:
13(7), P. 2452 - 2452
Published: July 18, 2021
Here
we
present
an
extensive
narrative
review
of
the
broadly
understood
modifications
to
lifestyles
women
with
polycystic
ovary
syndrome
(PCOS).
The
PubMed
database
was
analyzed,
combining
PCOS
entries
causes,
diseases,
diet
supplementation,
lifestyle,
physical
activity,
and
use
herbs.
metabolic
pathways
leading
disturbances
in
lipid,
carbohydrate,
hormonal
metabolism
targeted
patients
are
described.
article
refers
sleep
disorders,
changes
mental
health
parameters,
causes
oxidative
stress
inflammation.
These
conditions
consistently
lead
occurrence
severe
diseases
suffering
from
diabetes,
fatty
degeneration
internal
organs,
infertility,
atherosclerosis,
cardiovascular
dysbiosis,
cancer.
modification
lifestyles,
patterns
proper
selection
nutrients,
pharmacological
natural
supplementation
form
herbs,
activity
have
been
proposed.
progress
consequences
largely
modifiable
depend
on
patient’s
approach,
although
take
into
account
also
genetic
determinants.
Molecules,
Journal Year:
2021,
Volume and Issue:
26(5), P. 1417 - 1417
Published: March 5, 2021
Cancer
is
one
of
the
most
fatal
diseases
with
an
increasing
incidence
and
mortality
all
over
world.
Thus,
there
urgent
need
for
novel
therapies
targeting
major
cancer-related
pathways.
Nuclear
factor-erythroid
2-related
factor
2
(NRF2)
its
negative
modulator
Kelch-like
ECH-associated
protein
1
(KEAP1)
are
main
players
cellular
defense
mechanisms
against
internal
external
cell
stressors.
However,
NRF2/KEAP1
signaling
pathway
dysregulated
in
various
cancers,
thus
promoting
tumor
survival
metastasis.
In
present
review,
we
discuss
normal
deregulated
NRF2
focusing
on
functions.
We
further
explore
activators
inhibitors
this
as
cancer
drug
candidates
order
to
provide
extensive
background
subject.
Cell Communication and Signaling,
Journal Year:
2022,
Volume and Issue:
20(1)
Published: June 30, 2022
Abstract
NF-E2-related
factor
2
(Nrf2)
protein
is
a
basic-region
leucine
zipper
transcription
that
defends
against
endogenous
or
exogenous
stressors.
By
inducing
several
cytoprotective
and
detoxifying
gene
expressions,
Nrf2
can
increase
the
sensitivity
of
cells
to
oxidants
electrophiles.
Transient
activation,
by
its
specific
activators,
has
protective
roles
carcinogenesis
cancer
development.
However,
permanent
activation
promotes
various
properties,
comprising
malignant
progression,
chemo/radio
resistance,
poor
patient
prognosis.
Taken
together,
these
findings
suggest
reaching
an
optimal
balance
between
paradoxical
functions
in
malignancy
may
render
selective
improvement
identify
therapeutic
strategies
treatment.
In
this
review,
we
describe
lately
discovered
inducers
inhibitors,
their
chemopreventive
and/or
anticancer
activities.
Medicinal Research Reviews,
Journal Year:
2023,
Volume and Issue:
43(3), P. 614 - 682
Published: Jan. 19, 2023
Abstract
Ferroptosis
is
an
iron‐dependent
cell
death
program
that
characterized
by
excessive
lipid
peroxidation.
Triggering
ferroptosis
has
been
proposed
as
a
promising
strategy
to
fight
cancer
and
overcome
drug
resistance
in
antitumor
therapy.
Understanding
the
molecular
interactions
structural
features
of
ferroptosis‐inducing
compounds
might
therefore
open
door
efficient
pharmacological
strategies
against
aggressive,
metastatic,
therapy‐resistant
cancer.
We
here
summarize
mechanisms
requirements
small
molecules
target
central
players
ferroptosis.
Focus
placed
on
(i)
glutathione
peroxidase
(GPX)
4,
only
GPX
isoenzyme
detoxifies
complex
membrane‐bound
hydroperoxides,
(ii)
cystine/glutamate
antiporter
system
X
c
−
for
regeneration,
(iii)
redox‐protective
transcription
factor
nuclear
erythroid
2‐related
(NRF2),
(iv)
GPX4
repression
combination
with
induced
heme
degradation
via
oxygenase‐1.
deduce
common
ferroptotic
activity
highlight
challenges
development.
Moreover,
we
critically
discuss
potential
natural
products
lead
structures
provide
comprehensive
overview
structurally
diverse
biogenic
bioinspired
trigger
iron
oxidation,
inhibition
thioredoxin/thioredoxin
reductase
or
less
defined
modes
action.
Antioxidants,
Journal Year:
2024,
Volume and Issue:
13(1), P. 70 - 70
Published: Jan. 2, 2024
Physiological
concentrations
of
reactive
oxygen
species
(ROS)
play
vital
roles
in
various
normal
cellular
processes,
whereas
excessive
ROS
generation
is
central
to
disease
pathogenesis.
The
nuclear
factor
erythroid
2-related
2
(NRF2)
a
critical
transcription
that
regulates
the
antioxidant
systems
response
oxidative
stress
by
governing
expression
genes
encoding
enzymes
shield
cells
from
diverse
alterations.
NRF2
and
its
negative
regulator
Kelch-like
ECH-associated
protein
1
(KEAP1)
have
been
focus
numerous
investigations
elucidating
whether
suppresses
tumor
promotion
or
conversely
exerts
pro-oncogenic
effects.
has
found
participate
pathological
including
dysregulated
cell
proliferation,
metabolic
remodeling,
resistance
apoptosis.
Herein,
this
review
article
will
examine
intriguing
role
phase
separation
activating
transcriptional
activity
explore
dual
impacts
on
immunology,
cancer
stem
cells,
metastasis,
long
non-coding
RNAs
(LncRNAs).
Taken
together,
aims
discuss
multifaceted
both
prevention
while
also
addressing
advantages,
disadvantages,
limitations
associated
with
modulating
therapeutically
treatment.
Advanced Science,
Journal Year:
2024,
Volume and Issue:
11(16)
Published: Feb. 21, 2024
Abstract
Cancer
cells
typically
display
redox
imbalance
compared
with
normal
due
to
increased
metabolic
rate,
accumulated
mitochondrial
dysfunction,
elevated
cell
signaling,
and
accelerated
peroxisomal
activities.
This
may
regulate
gene
expression,
alter
protein
stability,
modulate
existing
cellular
programs,
resulting
in
inefficient
treatment
modalities.
Therapeutic
strategies
targeting
intra‐
or
extracellular
states
of
cancer
at
varying
state
progression
trigger
programmed
death
if
exceeded
a
certain
threshold,
enabling
therapeutic
selectivity
overcoming
resistance
radiotherapy
chemotherapy.
Nanotechnology
provides
new
opportunities
for
modulating
their
excellent
designability
high
reactivity.
Various
nanomaterials
are
widely
researched
enhance
highly
reactive
substances
(free
radicals)
production,
disrupt
the
endogenous
antioxidant
defense
systems,
both.
Here,
physiological
features
described
challenges
illustrated.
Then,
that
classified
elaborated
upon
based
on
ability
target
regulations.
Finally,
future
perspectives
this
field
proposed.
It
is
hoped
review
guidance
design
nanomaterials‐based
approaches
involving
therapy,
especially
cancers
resistant
chemotherapy,
etc.
Journal of Biological Chemistry,
Journal Year:
2024,
Volume and Issue:
300(4), P. 106793 - 106793
Published: Feb. 24, 2024
RNA
5-methylcytosine
(m5C)
is
an
abundant
chemical
modification
in
mammalian
RNAs
and
plays
crucial
roles
regulating
vital
physiological
pathological
processes,
especially
cancer.
However,
the
dysregulation
of
m5C
its
underlying
mechanisms
non-small
cell
lung
cancer
(NSCLC)
remain
unclear.
Here
we
identified
that
NSUN2,
a
key
methyltransferase,
highly
expressed
NSCLC
tumor
tissue.
We
found
elevated
NSUN2
expression
levels
strongly
correlate
with
grade
size,
predicting
poor
outcomes
for
patients.
Furthermore,
RNA-seq
subsequent
confirmation
studies
revealed
antioxidant-promoting
transcription
factor
NRF2
target
depleting
decreases
increases
sensitivity
cells
to
ferroptosis
activators
both
vitro
vivo.
Intriguingly,
methylated-RIP-qPCR
assay
results
indicated
mRNA
has
higher
level
when
overexpressed
but
shows
no
significant
changes
methyltransferase-deficient
group.
Mechanistically,
confirmed
upregulates
by
enhancing
stability
through
within
5'UTR
region
recognized
specific
reader
protein
YBX1,
rather
than
influencing
translation.
In
rescue
experiments,
show
knocking
down
diminished
proliferation,
migration,
tolerance
mediated
overexpression.
conclusion,
our
study
unveils
novel
regulatory
mechanism
which
sustains
m5C-YBX1-axis,
suggesting
targeting
regulated
pathway
might
offer
promising
therapeutic
strategies
Biomedicine & Pharmacotherapy,
Journal Year:
2020,
Volume and Issue:
131, P. 110676 - 110676
Published: Aug. 25, 2020
Chemoresistance
is
a
central
cause
for
the
tumor
management
failure.
Cancer
cells
disrupt
redox
homeostasis
through
reactive
oxygen
species
(ROS)
regulatory
mechanisms,
leading
to
progression
and
chemoresistance.
The
transcription
factor
nuclear
erythroid
2-related
2
(NRF2)
master
regulator
of
neutralizing
cellular
ROS
restoring
balance.
Understanding
role
NRF2
in
ROS-mediated
chemoresistance
can
be
helpful
development
chemotherapy
strategies
with
better
efficiency.
In
this
review,
we
sum
up
roles
classical
agents
including
cisplatin,
5-fluorouracil,
gemcitabine,
oxaliplatin,
paclitaxel,
doxorubicin,
how
overcome
by
targeting
NRF2.
Finally,
propose
that
might
promising
strategy
resist
ROS-driven
acquire
efficacy
cancer
treatment.
