Novel Insights into T-Cell Exhaustion and Cancer Biomarkers in PDAC Using Single Cell RNA Sequencing
bioRxiv (Cold Spring Harbor Laboratory),
Год журнала:
2025,
Номер
unknown
Опубликована: Янв. 15, 2025
Abstract
One
of
the
aggressive
and
lethal
cancers,
Pancreatic
ductal
adenocarcinoma
(PDAC)
is
characterised
by
poor
prognosis
resistance
to
conventional
treatments.
Moreover,
tumor
immune
microenvironment
(TIME)
plays
a
crucial
role
in
progression
therapeutic
PDAC.
It
associated
with
T-cells
exhaustion,
leading
progressive
loss
T-cell
functions
impaired
ability
kill
cells.
Therefore,
this
study
employed
single
cell
RNA
sequencing
(scRNA-seq)
analysis
identifying
upregulated
genes
T-cells;
cancer
cells
two
groups
(“cancer
cells_vs_all-PDAC”
“cancer-PDAC_vs_all-normal”).
Common
unique
markers
from
both
were
identified.
The
Reactome
pathways
selected;
while
implicated
those
used
perform
PPI
analysis,
revealing
hub-genes
T-cells.
gene
expression
validation
was
performed
using
GEPIA2
TISCH2,
overall
survival
GEPIA2.
Conclusively,
unravelled
16
novel
providing
groundwork
for
future
research
into
landscape
PDAC,
particularly
exhaustion.
However,
further
clinical
studies
are
needed
validate
these
as
potential
targets
PDAC
patients.
Graphical
abstract
Язык: Английский
DDX21 Controls Cell Cycle Progression and Autophagy in Pancreatic Cancer Cells
Cancers,
Год журнала:
2025,
Номер
17(4), С. 570 - 570
Опубликована: Фев. 7, 2025
Background:
Pancreatic
ductal
adenocarcinoma
(PDAC)
is
a
highly
lethal
cancer.
Late
diagnosis
and
acquisition
of
chemoresistance
contribute
to
its
dismal
prognosis.
While
surgical
resection
improved
the
clinical
outcome
patients,
only
~20%
them
are
eligible
due
advanced
disease
at
diagnosis.
Thus,
development
new
therapeutic
approaches
master
priority
for
an
management
this
The
helicase
DDX21
was
proposed
as
prognostic
marker
in
several
tumors,
including
PDAC.
Methods:DDX21
expression
evaluated
PDAC
samples
cell
lines;
RNA
sequencing
bioinformatics
analyses
DDX21-depleted
PANC-1
silenced
cells;
functional
autophagy,
cycle
proliferation.
Results:
expressed
higher
levels
liver
metastasis
patients.
Transcriptomics
cells
revealed
enrichment
genes
involved
autophagy
progression.
inactivation
by
interference
enhanced
basal
autophagic
flux
altered
reducing
rate
G1-S
transition.
Coherently,
proliferation
clonogenic
activity
significantly
reduced.
Conclusions:
Our
results
support
oncogenic
role
uncover
regulation
autophagy.
Язык: Английский