Cancer Communications,
Год журнала:
2022,
Номер
42(9), С. 848 - 867
Опубликована: Июль 29, 2022
Abstract
Background
Abnormal
expression
of
protein
tyrosine
phosphatases
(PTPs)
has
been
reported
to
be
a
crucial
cause
cancer.
As
member
PTPs,
phosphatase
receptor
type
O
(PTPRO)
revealed
play
tumor
suppressive
roles
in
several
cancers,
while
its
colorectal
cancer
(CRC)
remains
elucidated.
Hence,
we
aimed
explore
the
and
mechanisms
PTPRO
CRC
initiation
progression.
Methods
The
influences
on
growth
liver
metastasis
cells
patterns
different
lipid
metabolism
enzymes
were
evaluated
vitro
vivo.
Molecular
biological
experiments
conducted
uncover
underpinning
dysregulated
de
novo
lipogenesis
fatty
acid
β‐oxidation.
Results
was
notably
downregulated
compared
primary
cancer,
such
downregulation
associated
with
poor
prognosis
patients
CRC.
silencing
significantly
promoted
cell
metastasis.
Compared
wild‐type
mice,
PTPRO‐knockout
mice
developed
more
tumors
harbored
larger
loads
under
treatment
azoxymethane
dextran
sulfate
sodium.
Gene
set
enrichment
analysis
that
pathways.
Blockage
synthesis
abrogated
effects
Further
indicated
induced
activation
AKT
serine/threonine
kinase
(AKT)/mammalian
target
rapamycin
(mTOR)
signaling
axis,
thus
promoting
by
enhancing
sterol
regulatory
element‐binding
1
(SREBP1)
lipogenic
enzyme
acetyl‐CoA
carboxylase
alpha
(ACC1)
activating
AKT/mTOR
pathway.
Furthermore,
attenuation
decreased
oxidation
rate
repressing
peroxisome
proliferator‐activated
(PPARα)
downstream
peroxisomal
acyl‐coenzyme
A
oxidase
(ACOX1)
via
p38/extracellular
signal‐regulated
(ERK)
mitogen‐activated
(MAPK)
Conclusions
could
suppress
development
modulating
AKT/mTOR/SREBP1/ACC1
MAPK/PPARα/ACOX1
pathways
reprogramming
metabolism.
Journal of Clinical Investigation,
Год журнала:
2024,
Номер
134(2)
Опубликована: Янв. 15, 2024
Immunometabolism
is
a
burgeoning
field
of
research
that
investigates
how
immune
cells
harness
nutrients
to
drive
their
growth
and
functions.
Myeloid
play
pivotal
role
in
tumor
biology,
yet
metabolic
influence
on
antitumor
responses
remains
inadequately
understood.
This
Review
explores
the
landscape
tumor-associated
macrophages,
including
immunoregulatory
roles
glucose,
fatty
acids,
glutamine,
arginine,
alongside
tools
used
perturb
metabolism
promote
immunity.
The
confounding
inhibitors
our
interpretation
myeloid
phenotypes
will
also
be
discussed.
A
binary
schema
currently
describe
macrophage
immunological
phenotypes,
characterizing
inflammatory
M1
as
supported
by
glycolysis,
immunosuppressive
M2
oxidative
phosphorylation.
However,
this
classification
likely
underestimates
variety
states
vivo.
Understanding
these
nuances
critical
when
developing
interventional
strategies.
Future
should
focus
refining
drug
specificity
targeted
delivery
methods
maximize
therapeutic
efficacy.
Metabolic
alterations,
a
hallmark
of
cancer,
enable
tumor
cells
to
adapt
their
environment
by
modulating
glucose,
lipid,
and
amino
acid
metabolism,
which
fuels
rapid
growth
contributes
treatment
resistance.
In
primary
breast
metabolic
shifts
such
as
the
Warburg
effect
enhanced
lipid
synthesis
are
closely
linked
chemotherapy
failure.
Similarly,
metastatic
lesions
often
display
distinct
profiles
that
not
only
sustain
but
also
confer
resistance
targeted
therapies
immunotherapies.
The
review
emphasizes
two
major
aspects:
mechanisms
driving
in
both
how
unique
environments
sites
further
complicate
treatment.
By
targeting
vulnerabilities
at
stages,
new
strategies
could
improve
efficacy
existing
provide
better
outcomes
for
cancer
patients.
Signal Transduction and Targeted Therapy,
Год журнала:
2025,
Номер
10(1)
Опубликована: Фев. 20, 2025
The
progression
of
malignant
tumors
leads
to
the
development
secondary
in
various
organs,
including
bones,
brain,
liver,
and
lungs.
This
metastatic
process
severely
impacts
prognosis
patients,
significantly
affecting
their
quality
life
survival
rates.
Research
efforts
have
consistently
focused
on
intricate
mechanisms
underlying
this
corresponding
clinical
management
strategies.
Consequently,
a
comprehensive
understanding
biological
foundations
tumor
metastasis,
identification
pivotal
signaling
pathways,
systematic
evaluation
existing
emerging
therapeutic
strategies
are
paramount
enhancing
overall
diagnostic
treatment
capabilities
for
tumors.
However,
current
research
is
primarily
metastasis
within
specific
cancer
types,
leaving
significant
gaps
our
complex
cascade,
organ-specific
tropism
mechanisms,
targeted
treatments.
In
study,
we
examine
sequential
processes
elucidate
driving
organ-tropic
systematically
analyze
tumors,
those
tailored
organ
involvement.
Subsequently,
synthesize
most
recent
advances
technologies
challenges
opportunities
encountered
pertaining
bone
metastasis.
Our
objective
offer
insights
that
can
inform
future
practice
crucial
field.
Cancer Communications,
Год журнала:
2022,
Номер
42(9), С. 848 - 867
Опубликована: Июль 29, 2022
Abstract
Background
Abnormal
expression
of
protein
tyrosine
phosphatases
(PTPs)
has
been
reported
to
be
a
crucial
cause
cancer.
As
member
PTPs,
phosphatase
receptor
type
O
(PTPRO)
revealed
play
tumor
suppressive
roles
in
several
cancers,
while
its
colorectal
cancer
(CRC)
remains
elucidated.
Hence,
we
aimed
explore
the
and
mechanisms
PTPRO
CRC
initiation
progression.
Methods
The
influences
on
growth
liver
metastasis
cells
patterns
different
lipid
metabolism
enzymes
were
evaluated
vitro
vivo.
Molecular
biological
experiments
conducted
uncover
underpinning
dysregulated
de
novo
lipogenesis
fatty
acid
β‐oxidation.
Results
was
notably
downregulated
compared
primary
cancer,
such
downregulation
associated
with
poor
prognosis
patients
CRC.
silencing
significantly
promoted
cell
metastasis.
Compared
wild‐type
mice,
PTPRO‐knockout
mice
developed
more
tumors
harbored
larger
loads
under
treatment
azoxymethane
dextran
sulfate
sodium.
Gene
set
enrichment
analysis
that
pathways.
Blockage
synthesis
abrogated
effects
Further
indicated
induced
activation
AKT
serine/threonine
kinase
(AKT)/mammalian
target
rapamycin
(mTOR)
signaling
axis,
thus
promoting
by
enhancing
sterol
regulatory
element‐binding
1
(SREBP1)
lipogenic
enzyme
acetyl‐CoA
carboxylase
alpha
(ACC1)
activating
AKT/mTOR
pathway.
Furthermore,
attenuation
decreased
oxidation
rate
repressing
peroxisome
proliferator‐activated
(PPARα)
downstream
peroxisomal
acyl‐coenzyme
A
oxidase
(ACOX1)
via
p38/extracellular
signal‐regulated
(ERK)
mitogen‐activated
(MAPK)
Conclusions
could
suppress
development
modulating
AKT/mTOR/SREBP1/ACC1
MAPK/PPARα/ACOX1
pathways
reprogramming
metabolism.
