Cell Death and Disease,
Journal Year:
2022,
Volume and Issue:
13(11)
Published: Nov. 4, 2022
Metastasis
is
the
dominant
cause
of
cancer-related
mortality.
Metastasis-associated
with
colon
cancer
protein
1
(MACC1)
has
been
proven
to
play
a
critical
role
in
metastasis.
However,
prometastatic
MACC1
regulating
pancreatic
(PC)
metastatic
phenotype
remains
elusive.
Here,
we
report
that
highly
expressed
The
Cancer
Genome
Atlas
(TCGA)
and
tissue
microarray
(TMA)
identified
as
good
indicator
for
poor
prognosis.
Overexpression
or
knockdown
PC
cells
correspondingly
promoted
inhibited
cell
migration
invasion
MET
proto-oncogene
receptor
tyrosine
kinase
(MET)-independent
manner.
Notably,
markedly
decreased
liver
lesions
metastasis
model.
Mechanistically,
binds
epithelial-mesenchymal
transition
(EMT)
regulator
snail
family
transcriptional
repressor
(SNAI1)
drive
EMT
via
upregulating
activity
SNAI1,
leading
transactivation
fibronectin
(FN1)
trans-repression
cadherin
(CDH1).
Collectively,
our
results
unveil
new
mechanism
by
which
drives
suggest
MACC1-SNAI1
complex-mediated
mesenchymal
may
be
therapeutic
target
cancer.
Biomedicines,
Journal Year:
2023,
Volume and Issue:
11(6), P. 1611 - 1611
Published: June 1, 2023
Cancer
is
a
significant
challenge
for
effective
treatment
due
to
its
complex
mechanism,
different
progressing
stages,
and
lack
of
adequate
procedures
screening
identification.
Pancreatic
cancer
typically
identified
in
advanced
progression
phase
with
low
survival
~5
years.
Among
cancers,
pancreatic
also
considered
high
mortality-causing
casualty
over
other
accidental
or
disease-based
mortality,
it
ranked
seventh
among
all
mortality-associated
cancers
globally.
Henceforth,
developing
diagnostic
early
detection,
understanding
cancer-linked
mechanisms,
various
therapeutic
strategies
are
crucial.
This
review
describes
the
recent
development
progression,
approaches,
including
molecular
techniques
biomedicines
effectively
treating
cancer.
Cancer Letters,
Journal Year:
2024,
Volume and Issue:
585, P. 216640 - 216640
Published: Jan. 28, 2024
Gemcitabine,
a
pivotal
chemotherapeutic
agent
for
pancreatic
ductal
adenocarcinoma
(PDAC),
frequently
encounters
drug
resistance,
posing
significant
clinical
challenge
with
implications
PDAC
patient
prognosis.
In
this
study,
employing
an
integrated
approach
involving
bioinformatic
analyses
from
multiple
databases,
we
unveil
CSNK2A1
as
key
regulatory
factor.
The
patient-derived
xenograft
(PDX)
model
further
substantiates
the
critical
role
of
in
gemcitabine
resistance
within
context
PDAC.
Additionally,
targeted
silencing
expression
significantly
enhances
sensitivity
cells
to
treatment.
Mechanistically,
CSNK2A1's
transcriptional
regulation
is
mediated
by
H3K27
acetylation
Moreover,
identify
activator
autophagy,
and
enhanced
autophagy
drives
resistance.
Silmitasertib,
established
inhibitor,
can
effectively
inhibit
autophagy.
Notably,
combinatorial
treatment
Silmitasertib
demonstrates
remarkable
efficacy
treating
summary,
our
study
reveals
potent
predictive
factor
inhibition
represents
promising
therapeutic
strategy
restore
PDAC,
offering
hope
improved
outcomes.
Cells,
Journal Year:
2024,
Volume and Issue:
13(11), P. 948 - 948
Published: May 30, 2024
With
the
lack
of
specific
signs
and
symptoms,
pancreatic
ductal
adenocarcinoma
(PDAC)
is
often
diagnosed
at
late
metastatic
stages,
resulting
in
poor
survival
outcomes.
Among
various
biomarkers,
microRNA-21
(miR-21),
a
small
non-coding
RNA,
highly
expressed
PDAC.
By
inhibiting
regulatory
proteins
3′
untranslated
regions
(UTR),
miR-21
holds
significant
roles
PDAC
cell
proliferation,
epithelial–mesenchymal
transition,
angiogenesis,
as
well
cancer
invasion,
metastasis,
resistance
therapy.
We
conducted
systematic
search
across
major
databases
for
articles
on
mainly
published
within
last
decade,
focusing
their
diagnostic,
prognostic,
therapeutic,
biological
roles.
This
rigorous
approach
ensured
comprehensive
review
miR-21’s
multifaceted
role
cancers.
In
this
review,
we
explore
current
understandings
future
directions
regarding
regulation,
therapeutic
potential
targeting
exhaustive
discusses
involvement
transition
(EMT),
apoptosis
modulation,
its
therapy
resistance.
Also
discussed
interplay
between
molecular
pathways
that
contribute
to
tumor
progression,
with
reference
adenocarcinoma.
Cell Death and Disease,
Journal Year:
2022,
Volume and Issue:
13(11)
Published: Nov. 4, 2022
Metastasis
is
the
dominant
cause
of
cancer-related
mortality.
Metastasis-associated
with
colon
cancer
protein
1
(MACC1)
has
been
proven
to
play
a
critical
role
in
metastasis.
However,
prometastatic
MACC1
regulating
pancreatic
(PC)
metastatic
phenotype
remains
elusive.
Here,
we
report
that
highly
expressed
The
Cancer
Genome
Atlas
(TCGA)
and
tissue
microarray
(TMA)
identified
as
good
indicator
for
poor
prognosis.
Overexpression
or
knockdown
PC
cells
correspondingly
promoted
inhibited
cell
migration
invasion
MET
proto-oncogene
receptor
tyrosine
kinase
(MET)-independent
manner.
Notably,
markedly
decreased
liver
lesions
metastasis
model.
Mechanistically,
binds
epithelial-mesenchymal
transition
(EMT)
regulator
snail
family
transcriptional
repressor
(SNAI1)
drive
EMT
via
upregulating
activity
SNAI1,
leading
transactivation
fibronectin
(FN1)
trans-repression
cadherin
(CDH1).
Collectively,
our
results
unveil
new
mechanism
by
which
drives
suggest
MACC1-SNAI1
complex-mediated
mesenchymal
may
be
therapeutic
target
cancer.
