FDX1 downregulation activates mitophagy and the PI3K/AKT signaling pathway to promote hepatocellular carcinoma progression by inducing ROS production
Redox Biology,
Journal Year:
2024,
Volume and Issue:
75, P. 103302 - 103302
Published: Aug. 6, 2024
Mitochondrial
dysfunction
and
metabolic
reprogramming
can
lead
to
the
development
progression
of
hepatocellular
carcinoma
(HCC).
Ferredoxin
1
(FDX1)
is
a
small
mitochondrial
protein
recent
studies
have
shown
that
FDX1
plays
an
important
role
in
tumor
cuproptosis,
but
its
HCC
still
elusive.
In
this
study,
we
aim
investigate
expression
novel
functions
HCC.
Language: Английский
SLC35A2 is a novel prognostic biomarker and promotes cell proliferation and metastasis via Wnt/β-catenin/EMT signaling pathway in breast cancer
Rushu Yan,
No information about this author
Tianwen Chen
No information about this author
Scientific Reports,
Journal Year:
2025,
Volume and Issue:
15(1)
Published: Jan. 2, 2025
Language: Английский
Xanthohumol Regulates Mitophagy in Osteosarcoma Cells via AMPK‐ULK1‐FUNDC1 Signaling Pathway
Qiaofeng Ge,
No information about this author
Zhiliang Yan,
No information about this author
Qian Tian
No information about this author
et al.
Phytotherapy Research,
Journal Year:
2025,
Volume and Issue:
unknown
Published: April 7, 2025
ABSTRACT
Osteosarcoma
(OS)
is
the
most
common
primary
bone
malignancy.
The
therapeutic
efficacy
for
OS
patients
has
remained
stagnant
in
recent
decades.
Xanthohumol
(XN),
a
flavonoid
naturally
found
hops,
demonstrated
significant
anticancer
properties
lung
and
breast
cancer.
However,
its
effect
on
underlying
molecular
mechanisms
remains
uncertain.
Therefore,
purpose
of
this
study
to
explore
relationship
between
XN
OS.
Firstly,
we
assessed
impact
cell
proliferation
migration
using
CCK‐8,
wound‐healing,
transwell,
clonogenicity
assays.
Subsequently,
examined
mitophagy
cells
through
flow
cytometry,
immunofluorescence,
transmission
electron
microscopy,
western
blot
analysis.
Finally,
constructed
siRNA
targeting
AMPK
validate
pathway.
In
vitro,
that
inhibited
concentration‐
time‐dependent
manner.
Furthermore,
induced
mitochondrial
damage
increased
reactive
oxygen
species
(ROS)
levels.
RNA‐seq
analysis
suggested
potential
pathway,
which
confirmed
experimentally
by
showing
reduced
ATP
levels,
altered
membrane
potential,
expression
Atg5,
Beclin‐1,
LC3
proteins.
Interestingly,
inhibitor
Mdivi‐1
reversed
caused
cells.
exerted
anti‐OS
effects
activation
AMPK‐ULK1‐FUNDC1
signaling
was
effectively
after
knockdown.
vivo,
subcutaneous
nude
mouse
model
without
any
organ
toxicity.
emerges
as
promising
pharmaceutical
agent
Language: Английский
Integrating network pharmacology and experimental validation to explore the mitophagy‐associated pharmacological mechanism of modified Shisiwei Jianzhong decoction against aplastic anemia
Yun Zhang,
No information about this author
Jun Wang,
No information about this author
Bo Wang
No information about this author
et al.
Biomedical Chromatography,
Journal Year:
2024,
Volume and Issue:
38(10)
Published: July 18, 2024
Abstract
The
aim
of
this
work
was
to
investigate
the
therapeutic
effect
modified
Shisiwei
Jianzhong
Decoction
(SJD)
on
aplastic
anemia
(AA)
and
its
potential
pharmacological
mechanism
from
perspective
mitophagy.
A
comprehensive
approach
combining
network
pharmacology,
mendelian
randomization,
molecular
docking
animal
experiments
applied
evaluate
properties
SJD
against
AA.
By
integrating
multiple
databases,
it
determined
that
exerted
AA
by
targeting
three
key
targets
[
mammalian
target
rapamycin
(
MTOR),
poly(ADP‐ribose)
polymerase
1
(PARP1)
Sirtuin
(SIRT1)]
through
four
core
compounds
(quercetin,
resveratrol,
genistein
curcumin).
Mendelian
randomization
analysis
identified
MTOR
as
a
risk
factor
for
occurrence
while
PARP1
protective
factor.
Results
showed
improved
peripheral
blood
counts
promoted
proliferation
hematopoietic
stem
cells.
Mechanistically,
SJD,
especially
at
high
dose,
played
role
in
activating
mitophagy‐related
proteins
PTEN
induced
kinase
(PINK1)/Parkin
inhibiting
phosphatidylinositol
3‐kinase
(PI3K)/protein
(AKT)/MTOR
pathway.
This
study
revealed
first
time
chemical
composition
effects
AA,
which
can
restore
function
results
provide
inspiration
clinical
application
traditional
Chinese
medicine
treatment.
Language: Английский
Identification of a novel mitophagy-related signature for predicting clinical prognosis and immunotherapy of osteosarcoma
Peichuan Xu,
No information about this author
Jiangminghao Zhao,
No information about this author
Wenrui Zhao
No information about this author
et al.
Research Square (Research Square),
Journal Year:
2024,
Volume and Issue:
unknown
Published: May 2, 2024
Abstract
Background
Osteosarcoma
(OS)
is
a
highly
aggressive
malignancy
characterized
by
poor
prognosis.
Mitochondrial
autophagy
(mitophagy)
has
been
implicated
in
tumor
initiation,
progression,
and
response
to
therapy,
highlighting
it
potential
prognostic
indicator
therapeutic
target
cancers.
Despite
this,
the
precise
mechanisms
underlying
mitophagy
osteosarcoma
remain
enigmatic.
This
research
aims
develop
mitophagy-associated
signature
guide
strategies
prognosis
estimations.
Methods
Clinical
transcriptome
data
for
patients
with
skeletal
muscle
tissue
were
retrieved
from
UCSC
Xena
GTEx.
Mitophagy-related
genes
(MRGs)
obtained
Kyoto
Encyclopedia
of
Genes
Genomes
(KEGG)
website.
A
predictive
risk
model
was
constructed
using
Least
Absolute
Shrinkage
Selection
Operator
(LASSO)
algorithm
Cox
regression
analysis.
To
delve
into
fundamental
gene
expression
mechanisms,
we
employed
Gene
Ontology
(GO),
KEGG,
Set
Enrichment
Analysis
(GSEA).
Moreover,
different
immune-related
activities
between
two
groups
investigated
ascertain
efficacy
immunotherapy.
Lastly,
functional
analysis
key
MRAS
carried
out
via
vitro
experiments
pan-cancer
small
molecule
drugs
that
may
screened
through
molecular
docking.
Results
Based
on
seven
mitophagy-related
signatures,
stratified
high-
low-risk
categories.
The
exhibited
strong
capability,
as
evidenced
Kaplan-Meier
analysis,
time-dependent
AUC,
Nomogram.
Notably,
compared
group,
individuals
high-risk
group
lower
stromal,
immune,
estimate
scores.The
infiltration
immune
cells
decreased.
Further
evidence
supporting
MRAS's
protective
role
against
shown
in
vitro,
where
upregulating
its
could
suppress
proliferation,
migration,
invasion
while
stimulating
their
apoptosis.
Pan-cancer
further
demonstrated
variety
tumors.
Conclusion
study
identified
elucidated
impact
cells.
Consequently,
opened
up
fresh
avenues
clinical
prediction
established
basis
precision
therapy
osteosarcoma.
Language: Английский
Mitochondrial dysfunction and programmed cell death in osteosarcoma
Ke Zhang,
No information about this author
Mingyang Jiang,
No information about this author
Kai-Cheng Liu
No information about this author
et al.
journal of nutritional oncology,
Journal Year:
2024,
Volume and Issue:
9(2), P. 37 - 45
Published: June 1, 2024
Abstract
Osteosarcoma
is
the
most
prevalent
primary
malignant
bone
tumor,
primarily
affecting
adolescents
aged
15–25
years.
It
characterized
by
a
high
recurrence
rate,
poor
prognosis,
and
lack
of
important
biomarkers.
Significant
mitochondrial
dysfunction
in
osteosarcoma
cells
has
been
widely
reported
recent
studies.
Dysfunctional
mitochondria
occupy
an
position
cellular
metabolic
reprogramming,
immune
microenvironment
regulation,
programmed
cell
death.
Therefore,
targeting
may
represent
new
mechanism
to
overcome
therapeutic
barriers
treatment
provides
crucial
target
molecules
for
further
development
targeted
therapies
immunotherapies.
The
present
article
summarizes
reports
links
it
various
death
mechanisms,
aiming
provide
basis
clinical
practice.
Language: Английский