Molecular Mapping in Head and Neck Adenoid Cystic Carcinoma by Pathological Grade Using Whole-exome Sequencing and Spatial Transcriptome
Yuelu Zhu,
No information about this author
Li Lin,
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Shun Wang
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et al.
Human Pathology,
Journal Year:
2025,
Volume and Issue:
unknown, P. 105758 - 105758
Published: March 1, 2025
Language: Английский
Identification of TEFM as a potential therapeutic target for LUAD treatment
Wenxuan Hu,
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Jian Yang,
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Kang Hu
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et al.
Journal of Translational Medicine,
Journal Year:
2024,
Volume and Issue:
22(1)
Published: July 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
Language: Английский
Aberrant SWI/SNF Complex Members Are Predominant in Rare Ovarian Malignancies—Therapeutic Vulnerabilities in Treatment-Resistant Subtypes
Cancers,
Journal Year:
2024,
Volume and Issue:
16(17), P. 3068 - 3068
Published: Sept. 3, 2024
SWI/SNF
(SWItch/Sucrose
Non-Fermentable)
is
the
most
frequently
mutated
chromatin-remodelling
complex
in
human
malignancy,
with
over
20%
of
tumours
having
a
mutation
member.
Mutations
specific
members
are
characteristic
rare
chemoresistant
ovarian
cancer
histopathological
subtypes.
Somatic
mutations
Language: Английский
Foxd3/SLC5A6 axis regulates apoptosis in LUAD cells by controlling mitochondrial biotin uptake
Chong Zheng,
No information about this author
Wenxuan Hu,
No information about this author
Danni Wu
No information about this author
et al.
Cellular Signalling,
Journal Year:
2024,
Volume and Issue:
125, P. 111473 - 111473
Published: Oct. 18, 2024
Language: Английский
SWItch/Sucrose Nonfermentable complex-deficient pulmonary neoplasms: clinicopathologic characteristics and outcomes to radiotherapy and immunotherapy
Yu Gu,
No information about this author
Songtao Lai,
No information about this author
Juan Yang
No information about this author
et al.
Translational Lung Cancer Research,
Journal Year:
2024,
Volume and Issue:
13(10), P. 2660 - 2672
Published: Oct. 1, 2024
The
SWItch/Sucrose
Nonfermentable
(SWI/SNF)
complex,
a
multi-subunit
chromatin
remodeler,
is
linked
to
aggressive
tumors
when
deficient.
Accurate
identification
of
SWI/SNF
expression
status
crucial
for
tailoring
targeted
therapies.
Previous
studies
on
the
efficacy
immunotherapy
SWI/SNF-deficient
(SWI/SNF-d)
pulmonary
primarily
focus
non-small
cell
lung
cancer
(NSCLC),
with
limited
data
other
modalities
like
radiotherapy.
This
study
aims
analyze
clinicopathological
characteristics
and
prognostic
factors
SWI/SNF-d
neoplasms,
including
NSCLC
undifferentiated
tumors,
evaluate
effectiveness
radiotherapy
immunotherapy,
providing
foundation
improved
treatment
strategies
assessments.
Language: Английский
ARID2 Deficiency Enhances Tumor Progression via ERBB3 Signaling in TFE3-Rearranged Renal Cell Carcinoma
Current Issues in Molecular Biology,
Journal Year:
2024,
Volume and Issue:
46(12), P. 13675 - 13695
Published: Dec. 2, 2024
TFE3-rearranged
Renal
Cell
Carcinoma
(TFE3-RCC)
is
an
aggressive
subtype
of
RCC
characterized
by
Xp11.2
rearrangement,
leading
to
TFE3
fusion
proteins
with
oncogenic
potential.
Despite
advances
in
understanding
its
molecular
biology,
effective
therapies
for
advanced
cases
remain
elusive.
This
study
investigates
the
role
ARID2,
a
component
SWI/SNF
chromatin
remodeling
complex,
TFE3-RCC.
Through
series
vitro
and
vivo
experiments,
we
confirmed
that
ARID2
acts
as
tumor
suppressor
knockout
(KO)
enhanced
TFE3-RCC
cell
migration,
proliferation,
growth.
Transcriptomic
analysis
revealed
ERBB3
key
target
gene
regulated
both
PRCC-TFE3
ARID2.
Chromatin
immunoprecipitation
(ChIP)
assays
demonstrated
directly
binds
upregulates
expression,
KO
further
enhancing
this
effect.
cells
exhibited
significant
expression
enrichment
MAPK
signaling
pathways.
These
also
showed
increased
activation
ERBB3,
EGFR,
selective
SRC
MAPK.
heightened
sensitivity
inhibitor
AZD8931
compared
their
wild-type
counterparts,
exhibiting
significantly
reduced
migration
proliferation
rates.
findings
suggest
PRCC-TFE3-ARID2-ERBB3
axis
plays
critical
pathogenesis
highlights
potential
targeting
ARID2-deficient
therapeutic
strategy.
provides
new
insights
into
mechanisms
suggests
avenues
precision
treatment
cancer.
Language: Английский
A Rare Case of Rhabdoid Pancreatic Carcinoma: Prolonged Disease-Free Survival Following Upfront Resection and Adjuvant Chemotherapy
Cureus,
Journal Year:
2023,
Volume and Issue:
unknown
Published: Dec. 7, 2023
The
rhabdoid
subtype
of
undifferentiated
pancreatic
carcinoma
is
rarely
reported.
clinical
course
this
disease
therefore
poorly
understood,
although
it
apparently
an
aggressive
malignancy.
We
herein
discuss
the
case
a
69-year-old
man
presenting
with
rapidly
enlarging
mass
body
and
tail
who
was
diagnosed
locally
advanced
SMARCB1-deficient
features,
treated
radical
resection
adjuvant
chemotherapy,
has
achieved
18-month
disease-free
survival
ongoing
at
time
article
publication.
identify
contrast
our
15
similar
tumors
reported
in
English
literature,
briefly
biology
tumor,
its
relationship
to
malignant
childhood,
role
SMARCB1
parent
complex
switch/sucrose-non-fermentable
chromatin
remodeling
(SWI/SNF)
modulating
behavior
malignancy,
potential
therapeutic
avenues
available
for
SWI/SNF-mutated
malignancies.
Language: Английский