Autophagy Deficiency Induced by SAT1 Potentiates Tumor Progression in Triple‐Negative Breast Cancer
Advanced Science,
Год журнала:
2024,
Номер
unknown
Опубликована: Июль 29, 2024
Aggressive
triple-negative
breast
cancer
(TNBC)
still
lacks
approved
targeted
therapies,
requiring
more
exploration
of
its
underlying
mechanisms.
Previous
studies
have
suggested
a
potential
role
SAT1
(Spermidine/Spermine
N1-acetyltransferase
1)
in
cancer,
which
needs
to
be
further
elucidated
cancer.
In
this
study,
highly
expressed
TNBC
signified
worse
patient
prognoses.
And
knockdown
effectively
inhibited
the
proliferation
and
migration
abilities
cells
vitro
vivo.
terms
mechanism,
transcription
factor
JUN
enhanced
transcriptional
activity
by
binding
promoter
region.
Then,
protein
cytoplasm
engaged
directly
with
YBX1
for
sustaining
stability
via
deubiquitylation
mediated
E3
ligase
HERC5.
Further,
was
found
suppress
autophagy
remarkably
stabilization
mTOR
mRNA
accumulation
YBX1-mediated
methyl-5-cytosine
(m5C)
modification.
These
findings
proved
that
drives
progression
through
SAT1/YBX1/mTOR
axis,
may
provide
candidate
therapy
advanced
TNBC.
Язык: Английский
E3 ligase HERC5-catalyzed UGDH isgylation promotes SNAI1-mediated tumor metastasis and cisplatin resistance in oral squamous cell carcinoma
Biology Direct,
Год журнала:
2025,
Номер
20(1)
Опубликована: Март 5, 2025
Oral
squamous
cell
carcinoma
(OSCC)
is
one
of
the
leading
causes
cancer-related
mortality
worldwide
due
to
its
high
aggressive
potential
and
drug
resistance.
Previous
studies
have
revealed
an
important
function
HECT
And
RLD
Domain
Containing
E3
Ubiquitin
Protein
Ligase
5
(HERC5)
in
cancer.
Six
GEO
gene
microarrays
identified
HERC5
as
a
significant
upregulated
OSCC
tissues
or
cells
(log2
Fold
change
>
1
adj.p
<
0.05).
This
study
aimed
explore
role
underlying
mechanisms
development.
High
expression
was
confirmed
by
our
hospital
validation
cohort
positively
correlated
with
primary
tumor
stages.
Subsequent
functional
demonstrated
that
knockdown
inhibited
migratory
invasive
capabilities
decrease
Vimentin
increase
E-cadherin
cells.
In
cisplatin
treatment,
survival
rates
were
significantly
reduced
HERC5-silencing
cells,
accompanied
cytotoxicity,
DNA
damage
apoptosis.
cell-derived
xenograft
displayed
depletion
pulmonary
metastasis
well
restored
cisplatin-induced
burden.
line
this,
overexpression
yielded
opposite
alterations
both
vivo
vitro.
Mechanistically,
UDP-glucose
6-dehydrogenase
(UGDH)
HERC5-binding
protein.
Cysteine
residue
at
position
994
domain
catalyzed
conjugation
ubiquitin-like
protein
Interferon-induced
15
kDa
(ISG15)
UGDH
(ISGylation
UGDH)
facilitated
phosphorylation,
therefore
enhancing
SNAI1
mRNA
stability.
overexpression-triggered
invasion
resistance
Our
indicates
may
be
promising
therapeutic
target
for
OSCC.
Язык: Английский
Cyclovirobuxine D Inhibits Triple-Negative Breast Cancer via YAP/TAZ Suppression and Activation of the FOXO3a/PINK1-Parkin Pathway-Induced Mitophagy
Phytomedicine,
Год журнала:
2024,
Номер
136, С. 156287 - 156287
Опубликована: Ноя. 26, 2024
Язык: Английский
SARS-CoV-2 nucleocapsid protein interaction with YBX1 displays oncolytic properties through PKM mRNA destabilization
Molecular Cancer,
Год журнала:
2024,
Номер
23(1)
Опубликована: Ноя. 6, 2024
SARS-CoV-2,
a
highly
contagious
coronavirus,
is
responsible
for
the
global
pandemic
of
COVID-19
in
2019.
Currently,
it
remains
uncertain
whether
SARS-CoV-2
possesses
oncogenic
or
oncolytic
potential
influencing
tumor
progression.
Therefore,
important
to
evaluate
clinical
and
functional
role
on
Here,
we
integrated
bioinformatic
analysis
RNA-seq
data
from
GEO
database
performed
studies
explore
regulatory
solid
progression,
including
lung,
colon,
kidney
liver
cancer.
Our
results
demonstrate
that
infection
with
associated
decreased
expression
genes
cancer
proliferation
metastasis
lung
tissues
patients
diagnosed
COVID-19.
Several
related
were
frequently
downregulated
infected
intestinal
organoids
human
colon
carcinoma
cells.
In
vivo
vitro
revealed
nucleocapsid
(N)
protein
inhibits
growth
through
N-terminal
(NTD)
C-terminal
domain
(CTD).
The
molecular
mechanism
indicates
N
interacts
YBX1,
resulting
recruitment
PKM
mRNA
into
stress
granules
mediated
by
G3BP1.
This
process
ultimately
destabilizes
suppresses
glycolysis.
study
reveals
new
function
Язык: Английский
Zingerone Facilitates Apoptosis in Triple Negative Breast Cancer Cells by Inducing Autophagy
Journal of Biochemical and Molecular Toxicology,
Год журнала:
2024,
Номер
38(12)
Опубликована: Дек. 1, 2024
ABSTRACT
Triple
negative
breast
cancer
(TNBC)
is
characterized
by
high
heterogenicity
and
aggressiveness
autophagy
plays
a
complicated
role
in
development.
Zingerone
reported
to
possess
multiple
pharmacological
activities,
including
antitumors.
This
study
explored
the
biological
relevant
mechanisms
of
zingerone
TNBC.
Following
treatment,
viability
normal
cells
MCF‐10A
TNBC
(MDA‐MB‐231
MDA‐MB‐468)
was
detected
with
CCK‐8
assay.
The
proliferation,
migration
invasion
were
colony
formation,
wound
healing,
transwell
assays.
Western
blot
used
detect
expressions
migration‐,
apoptosis‐
autophagy‐related
proteins.
Flow
cytometry
cell
apoptotic
level
immunofluorescence
assay
measured
autophagy.
experimental
data
revealed
that
varying
concentrations
suppressed
viability,
while
promoting
apoptosis
TNBC,
which
might
be
mediated
activation.
Besides,
decreased
HDAC1
expression
regulated
via
HDAC1.
Collectively,
impeded
malignant
progression
inducing
HDAC1‐mediated
Язык: Английский