Immunity Inflammation and Disease,
Год журнала:
2024,
Номер
12(2)
Опубликована: Фев. 1, 2024
Abstract
Introduction
Tumor‐associated
macrophages,
a
major
component
of
the
tumor
microenvironment,
undergo
polarization
into
M2
macrophages
(M2),
and
thereby
exert
an
immunosuppressive
effect
to
induce
cancer
metastasis.
This
study
strives
uncover
molecular
mechanism
underlying
this
event
in
hepatocellular
carcinoma
(HCC).
Methods
Proteasome
subunit
alpha
5
(PSMA5)
expression
liver
(LIHC)
tissues
its
association
with
LIHC
patients
were
predicted
using
StarBase.
PSMA5
level
human
HCC
cells
was
manipulated
via
transfection.
Exosomes
isolated
from
cells,
internalized
which
cocultured
cells.
Exosome
internalization
observed
after
fluorescence
labeling.
cell
migration
invasion
evaluated
by
wound
healing
Transwell
assays.
Xenograft
assay
performed
investigate
role
vitro
tumorigenesis.
assessed
enzyme‐linked
immunosorbent
assay,
quantitative
reverse
transcription
polymerase
chain
reaction,
immunohistochemistry.
exosomes
Janus
Kinase
2
(JAK2)/signal
transducer
activator
3
(STAT3)
activation
tumors
detected
Western
blot
analysis.
Results
High
associated
compromised
survival
patients.
knockdown
inhibited
invasion.
downregulated
these
cell‐isolated
successfully
facilitated
JAK2/STAT3
pathway
activation.
cell‐secreted
exosomal
exosome‐induced
on
attenuated
promotion
induced
exosome‐treated
migration/invasion
tumorigenesis
along
vivo
Conclusion
hinders
suppress
progression
restraining
signaling.
Abstract
The
tumor
microenvironment
(TME)
is
the
ecosystem
surrounding
a
tumor,
which
usually
consists
of
nontumoral
cells
or
components,
and
molecules
they
produce
release.
frequent
continuous
interplay
between
TME
strongly
affects
development,
disease
progression,
metastasis,
responses
to
therapeutic
interventions.
As
hub
potential
targets,
has
gained
appreciable
momentum
in
cancer
research.
Here
we
systematically
review
progress
targeting
as
strategy
develop
novel
antitumor
drugs
from
immunological,
stromal
extracellular
matrix
components
TME,
shedding
light
on
its
complex
synergies
with
cells.
This
exploration
highlights
transformative
these
elements
hold
refining
treatment
approaches.
thorough
examination
not
only
accentuates
TME's
multifaceted
nature
but
also
positions
it
formidable
avenue
for
propelling
forward
paradigms
therapy.
aims
foster
deeper
understanding
role
oncogenesis
exploitation
advancing
targeted,
efficacious
treatments,
marking
significant
stride
realm
Cell Death and Disease,
Год журнала:
2024,
Номер
15(4)
Опубликована: Апрель 4, 2024
Abstract
The
immunosuppressive
microenvironment
caused
by
several
intrinsic
and
extrinsic
mechanism
has
brought
great
challenges
to
the
immunotherapy
of
pancreatic
cancer.
We
identified
GFPT2,
key
enzyme
in
hexosamine
biosynthesis
pathway
(HBP),
as
an
immune-related
prognostic
gene
cancer
using
transcriptome
sequencing
further
confirmed
that
GFPT2
promoted
macrophage
M2
polarization
malignant
phenotype
HBP
is
a
glucose
metabolism
leading
generation
uridine
diphosphate
N-acetylglucosamine
(UDP-GlcNAc),
which
utilized
for
protein
O-GlcNAcylation.
GFPT2-mediated
O-GlcNAcylation
played
important
role
regulating
immune
microenvironment.
Through
cellular
proteomics,
we
IL-18
downstream
CO-IP
mass
spectrum,
YBX1
was
O-GlcNAcylated
nuclear
translocated
Then,
functioned
transcription
factor
promote
transcription.
Our
study
elucidated
relationship
between
metabolic
cells
microenvironment,
might
provide
some
insights
into
combination
therapy
vulnerability
Information
transmission
between
primary
tumor
cells
and
immunocytes
or
stromal
in
distal
organs
is
a
critical
factor
the
formation
of
pre-metastatic
niche
(PMN).
Understanding
this
mechanism
essential
for
developing
effective
therapeutic
strategy
against
metastasis.
Our
study
aims
to
prove
hypothesis
that
circ-0034880-enriched
tumor-derived
extracellular
vesicles
(TEVs)
mediate
PMN
colorectal
cancer
liver
metastasis
(CRLM),
targeting
TEVs
might
be
an
CRLM.
Immunity Inflammation and Disease,
Год журнала:
2024,
Номер
12(2)
Опубликована: Фев. 1, 2024
Abstract
Introduction
Tumor‐associated
macrophages,
a
major
component
of
the
tumor
microenvironment,
undergo
polarization
into
M2
macrophages
(M2),
and
thereby
exert
an
immunosuppressive
effect
to
induce
cancer
metastasis.
This
study
strives
uncover
molecular
mechanism
underlying
this
event
in
hepatocellular
carcinoma
(HCC).
Methods
Proteasome
subunit
alpha
5
(PSMA5)
expression
liver
(LIHC)
tissues
its
association
with
LIHC
patients
were
predicted
using
StarBase.
PSMA5
level
human
HCC
cells
was
manipulated
via
transfection.
Exosomes
isolated
from
cells,
internalized
which
cocultured
cells.
Exosome
internalization
observed
after
fluorescence
labeling.
cell
migration
invasion
evaluated
by
wound
healing
Transwell
assays.
Xenograft
assay
performed
investigate
role
vitro
tumorigenesis.
assessed
enzyme‐linked
immunosorbent
assay,
quantitative
reverse
transcription
polymerase
chain
reaction,
immunohistochemistry.
exosomes
Janus
Kinase
2
(JAK2)/signal
transducer
activator
3
(STAT3)
activation
tumors
detected
Western
blot
analysis.
Results
High
associated
compromised
survival
patients.
knockdown
inhibited
invasion.
downregulated
these
cell‐isolated
successfully
facilitated
JAK2/STAT3
pathway
activation.
cell‐secreted
exosomal
exosome‐induced
on
attenuated
promotion
induced
exosome‐treated
migration/invasion
tumorigenesis
along
vivo
Conclusion
hinders
suppress
progression
restraining
signaling.
