Oxidative Stress and Cancer Therapy: Controlling Cancer Cells Using Reactive Oxygen Species
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(22), С. 12387 - 12387
Опубликована: Ноя. 18, 2024
Cancer
is
a
multifaceted
disease
influenced
by
various
mechanisms,
including
the
generation
of
reactive
oxygen
species
(ROS),
which
have
paradoxical
role
in
both
promoting
cancer
progression
and
serving
as
targets
for
therapeutic
interventions.
At
low
concentrations,
ROS
serve
signaling
agents
that
enhance
cell
proliferation,
migration,
resistance
to
drugs.
However,
at
elevated
levels,
induce
oxidative
stress,
causing
damage
biomolecules
leading
death.
cells
developed
mechanisms
manage
activating
pathways
such
NRF2,
NF-κB,
PI3K/Akt.
This
review
explores
relationship
between
cancer,
focusing
on
death
like
apoptosis,
ferroptosis,
autophagy,
highlighting
potential
strategies
exploit
target
cells.
Язык: Английский
CRIP1 inhibits cutaneous melanoma progression through TFAM-mediated mitochondrial biogenesis
Scientific Reports,
Год журнала:
2025,
Номер
15(1)
Опубликована: Фев. 4, 2025
Язык: Английский
Deregulation of mitochondrial gene expression in cancer: mechanisms and therapeutic opportunities
British Journal of Cancer,
Год журнала:
2024,
Номер
131(9), С. 1415 - 1424
Опубликована: Авг. 14, 2024
Язык: Английский
Adipose Stem Cells and Their Interplay with Cancer Cells and Mitochondrial Reservoir: A New Promising Target
Cancers,
Год журнала:
2024,
Номер
16(15), С. 2769 - 2769
Опубликована: Авг. 5, 2024
Adipose-derived
stem
cells
(ASCs)
significantly
influence
tumor
progression
within
the
microenvironment
(TME).
This
review
examines
pro-tumorigenic
roles
of
ASCs,
focusing
on
paracrine
signaling,
direct
cell–cell
interactions,
and
immunomodulation.
ASC-mediated
mitochondrial
transfer
through
tunneling
nanotubes
(TNTs)
gap
junctions
(GJs)
plays
a
significant
role
in
enhancing
cancer
cell
survival
metabolism.
Cancer
with
dysfunctional
mitochondria
acquire
from
ASCs
to
meet
their
metabolic
needs
thrive
TME.
Targeting
transfer,
modulating
ASC
function,
influencing
pathways
are
potential
therapeutic
strategies.
However,
challenges
like
TME
complexity,
specificity,
safety
concerns,
resistance
mechanisms
must
be
addressed.
Disrupting
ASC–cancer
cell–mitochondria
axis
offers
promising
approach
therapy.
Язык: Английский
Mitochondrial DNA Alterations in Glioblastoma and Current Therapeutic Targets
Frontiers in Bioscience-Landmark,
Год журнала:
2024,
Номер
29(10)
Опубликована: Окт. 23, 2024
Metabolic
reprogramming
within
tumor
cells
involves
a
shift
towards
either
glycolysis
or
mitochondrial
respiration,
depending
on
the
stage
of
progression.
Consequently,
irreversible
dysfunction
mitochondria
is
considered
crucial
mechanism
driving
progression
mechanism.
While
numerous
mutations
in
DNA
(mtDNA)
have
been
identified
across
various
types,
including
glioblastoma,
many
studies
limited
scope,
focusing
small
segments
mtDNA
utilizing
sequencing
methods
with
restricted
sensitivity.
As
result,
several
potentially
significant
may
underestimated,
along
their
heteroplasmic
states,
which
play
role
determining
phenotypic
impact
mutation.
Although
both
somatic
and
germline
observed
different
research
linked
to
glioblastoma
remains
scarce.
The
genome
encodes
thirteen
protein-coding
genes
that
are
essential
for
proper
functioning
respiratory
complex
chains.
Alterations
function
manifest
at
levels,
structural
functional
changes,
impacting
mitogenic,
hemodynamic,
bioenergetic,
apoptotic
signaling
pathways.
These
alterations
often
signify
reduced
efficiency
oxidative
phosphorylation
system
energy
production
cells.
glioma
development
grows,
emerged
as
promising
targets
therapy
aimed
overcoming
chemoresistance
eliminating
cancer
This
brief
review
outlines
association
between
alteration
well
current
advancements
therapeutic
strategies
targeting
alterations.
Язык: Английский
Identification of TEFM as a potential therapeutic target for LUAD treatment
Journal of Translational Medicine,
Год журнала:
2024,
Номер
22(1)
Опубликована: Июль 29, 2024
Abstract
Background
Molecularly
targeted
therapies
have
recently
become
a
hotspot
in
the
treatment
of
LUAD,
with
ongoing
efforts
to
identify
new
effective
targets
due
individual
variability.
Among
these
potential
targets,
mitochondrial
transcription
elongation
factor
(TEFM)
stands
out
as
crucial
molecule
involved
synthetic
transcriptional
processing.
Dysregulation
TEFM
has
been
implicated
development
various
diseases;
however,
its
specific
role
LUAD
remains
unclear.
Methods
We
conducted
comprehensive
analysis
expression
leveraging
data
from
TCGA
database.
Subsequently,
we
validated
findings
using
clinical
specimens
obtained
First
Affiliated
Hospital
Soochow
University,
employing
western
blotting
and
qRT-PCR
techniques.
Further
experimental
validation
was
performed
through
transfection
cells
overexpression,
knockdown,
knockout
lentiviruses.
The
effects
on
were
evaluated
both
vitro
vivo
range
assays,
including
CCK-8,
colony
formation,
EdU
incorporation,
Transwell
migration,
Tunel
assay,
flow
cytometry,
JC-1
staining,
xenograft
tumour
models.
Results
Our
investigation
uncovered
that
exhibited
elevated
levels
co-localization
mitochondria.
Overexpression
facilitated
malignant
processes
cells,
whereas
silencing
notably
curbed
behaviors
induced
depolarization,
along
ROS
production,
culminating
apoptosis.
Moreover,
absence
substantially
influenced
transcripts
respiratory
chain
complexes.
nude
mouse
tumors
further
inhibiting
markedly
hindered
tumor
growth.
Conclusion
promotes
progression
EMT
pathway
determines
apoptosis
by
affecting
complexes,
providing
therapeutic
direction
for
LUAD-targeted
therapy.
Graphical
Язык: Английский
A turn-on mitochondria-targeted iridium (Ⅲ) Complex-Based probe for glutathione detection and photodynamic therapy of cancer cells
Spectrochimica Acta Part A Molecular and Biomolecular Spectroscopy,
Год журнала:
2024,
Номер
329, С. 125579 - 125579
Опубликована: Дек. 11, 2024
Язык: Английский
Adenine nucleotide translocase 2 silencing promotes metabolic adaptations and anoikis in P19 embryonal carcinoma stem cells
bioRxiv (Cold Spring Harbor Laboratory),
Год журнала:
2024,
Номер
unknown
Опубликована: Июнь 9, 2024
Abstract
Cancer
stem
cells
(CSCs)
are
amongst
the
group
of
constituting
tumors,
being
characterized
by
their
strong
self-renewal
and
survival
properties.
cells,
CSCs
included,
thought
to
rely
mostly
on
glycolysis,
even
in
presence
oxygen,
which
confers
them
adaptative
advantages.
Adenine
nucleotide
translocator
2
(ANT2),
responsible
for
exchange
ADP
ATP
mitochondrial
inner
membrane,
has
been
correlated
with
a
higher
glycolytic
metabolism
is
known
be
overexpressed
cancer
cells.
Using
P19
embryonal
carcinoma
(P19SCs)
as
model,
we
inhibit
ANT2
translation
using
siRNA.
protein
levels
were
shown
P19SC
when
compared
differentiated
counterparts.
Furthermore,
showed
here
that
OXPHOS
machinery
membrane
potential
compromised
after
depletion,
exhibiting
metabolic
adaptation
towards
less
oxidative
phenotype.
Interestingly,
hexokinase
II
downregulated,
was
also
accompanied
decreased
cell
growth,
ability
form
spheroids.
Our
findings
underscore
key
regulator
remodeling
CSCs,
suggesting
its
therapeutic
target
controlling
CSC-driven
tumor
progression.
Highlights
silencing
promotes
growth
arrest
CSCs.
depletion
modulates
HKII
levels.
induce
anoikis
resistance
P19SCs
Язык: Английский
Cancerous Conditions Accelerate the Aging of Skeletal Muscle via Mitochondrial DNA Damage
Yi Luo,
Rina Fujiwara‐Tani,
Isao Kawahara
и другие.
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(13), С. 7060 - 7060
Опубликована: Июнь 27, 2024
Skeletal
muscle
aging
and
sarcopenia
result
in
similar
changes
the
levels
of
markers.
However,
few
studies
have
examined
cancer
from
perspective
aging.
Therefore,
this
study
investigated
explored
its
causes
vitro
vivo.
In
mouse
aging,
cachexia,
cachexia
models,
skeletal
muscles
showed
markers
including
oxidative
stress,
fibrosis,
reduced
differentiation
potential,
telomere
shortening.
Furthermore,
examination
mitochondrial
DNA
revealed
a
5
kb
deletion
major
arc;
truncation
complexes
I,
IV,
V
electron
transport
chain;
phosphorylation
(OXPHOS).
The
model
demonstrated
high
high-mobility
group
box-1
(HMGB1)
tumor
necrosis
factor-α
(TNFα)
ascites.
Continuous
administration
neutralizing
antibodies
against
HMGB1
TNFα
stress
abrogated
deletion.
These
results
suggest
that
sarcopenia,
caused
by
inflammatory
cytokines
leads
to
damage,
which
turn
decreased
OXPHOS
promotion
Язык: Английский
CYP19A1 regulates chemoresistance in colorectal cancer through modulation of estrogen biosynthesis and mitochondrial function
Cancer & Metabolism,
Год журнала:
2024,
Номер
12(1)
Опубликована: Окт. 28, 2024
Abstract
Chemoresistance
remains
a
major
challenge
in
the
effective
treatment
of
colorectal
cancer
(CRC),
contributing
to
poor
patient
outcomes.
While
molecular
mechanisms
underlying
chemoresistance
are
complex
and
multifaceted,
emerging
evidence
suggests
that
altered
mitochondrial
function
hormone
signaling
play
crucial
roles.
In
this
study,
we
investigated
role
CYP19A1,
key
enzyme
estrogen
biosynthesis,
regulating
CRC.
Using
combination
vitro
functional
assays,
transcriptomic
analysis,
clinical
data
mining,
demonstrate
CYP19A1
expression
is
significantly
upregulated
CRC
cells
patient-derived
samples
compared
normal
controls.
Mechanistically,
found
regulates
through
modulation
I
activity,
which
mediated
by
CYP19A1-dependent
biosynthesis.
Notably,
targeted
inhibition
using
specific
inhibitors
effectively
reversed
chemotherapeutic
drugs.
Moreover,
analysis
TCGA
dataset
revealed
high
correlates
with
overall
survival
chemotherapy-treated
patients.
Taken
together,
our
findings
uncover
novel
for
signaling,
highlight
potential
targeting
CYP19A1/estrogen/complex
axis
as
therapeutic
strategy
overcome
improve
Язык: Английский