Frontiers in Oncology,
Journal Year:
2022,
Volume and Issue:
12
Published: June 15, 2022
Gastric
cancer
has
been
one
of
the
most
common
cancers
worldwide
with
extensive
metastasis
and
high
mortality.
Chemotherapy
found
as
a
main
treatment
for
metastatic
gastric
cancer,
whereas
drug
resistance
limits
effectiveness
chemotherapy
leads
to
failure.
in
complex
multifactorial
mechanism,
among
which
lipid
metabolism
plays
vital
role.
Increased
synthesis
new
lipids
or
uptake
exogenous
can
facilitate
rapid
growth
cells
tumor
formation.
Lipids
form
structural
basis
biofilms
while
serving
signal
molecules
energy
sources.
It
is
noteworthy
that
capable
inducing
by
reshaping
micro-environment.
In
this
study,
mechanisms
metabolic
pathways
correlated
are
reviewed.
particular,
we
discuss
effects
on
autophagy,
biomarkers
from
perspective
metabolism.
brief,
insights
be
gained
into
development
promising
therapies
through
an
in-depth
investigation
mechanism
reprogramming
resensitization
cells,
scientific
provided
applying
lipid-key
enzyme
inhibitors
chemical
sensitizers
clinical
settings.
Cancers,
Journal Year:
2021,
Volume and Issue:
13(5), P. 935 - 935
Published: Feb. 24, 2021
Collagen
type
XI
alpha
1
(COL11A1),
one
of
the
three
chains
collagen,
is
crucial
for
bone
development
and
collagen
fiber
assembly.
Interestingly,
COL11A1
expression
increased
in
several
cancers
high
levels
are
often
associated
with
poor
survival,
chemoresistance,
recurrence.
This
review
will
discuss
recent
discoveries
biological
functions
cancer.
predominantly
expressed
secreted
by
a
subset
cancer-associated
fibroblasts,
modulating
tumor-stroma
interaction
mechanical
properties
extracellular
matrix.
also
promotes
cancer
cell
migration,
metastasis,
therapy
resistance
activating
pro-survival
pathways
tumor
metabolic
phenotype.
Several
inhibitors
that
currently
being
tested
clinical
trials
or
used
clinic
other
diseases,
can
be
potentially
to
target
signaling.
Collectively,
this
underscores
role
as
promising
biomarker
key
player
Cancer Communications,
Journal Year:
2020,
Volume and Issue:
41(1), P. 16 - 36
Published: Nov. 10, 2020
Cancer
cells
are
abnormal
that
can
reproduce
and
regenerate
rapidly.
They
characterized
by
unlimited
proliferation,
transformation
migration,
destroy
normal
cells.
To
meet
the
needs
for
cell
proliferation
tumor
acquire
molecular
materials
energy
through
unusual
metabolic
pathways
as
their
metabolism
is
more
vigorous
than
of
Multiple
carcinogenic
signaling
eventually
converge
to
regulate
three
major
in
cells,
including
glucose,
lipid,
amino
acid
metabolism.
The
distinct
signatures
cancer
reflect
changes
indispensable
genesis
development
In
this
review,
we
report
unique
alterations
which
occur
various
axes,
present
modalities
available
diagnosis
clinical
therapy.
We
further
provide
suggestions
anti-tumor
therapeutic
drugs.
Cancer Letters,
Journal Year:
2020,
Volume and Issue:
473, P. 74 - 89
Published: Jan. 2, 2020
Gastrointestinal
cancer
causes
countless
deaths
every
year
due
to
therapeutic
resistance.
However,
whether
metabolic
alterations
contribute
chemoresistance
is
not
well
understood.
In
this
study,
we
report
that
fatty
acid
(FA)
catabolism
was
activated
in
gastrointestinal
cells
treated
with
oxaliplatin,
which
exhibited
higher
expression
of
the
rate-limiting
enzymes
carnitine
palmitoyltransferase
1B
(CPT1B)
and
CPT2.
The
clinical
analysis
also
showed
high
these
associated
poor
oxaliplatin-based
chemotherapy
outcomes
patients.
Furthermore,
genetic
or
pharmacological
inhibition
CPT2
perhexiline
disturbed
NADPH
redox
homeostasis
increased
reactive
oxygen
species
(ROS)
generation
cell
apoptosis
following
oxaliplatin
treatment.
Specifically,
combination
significantly
suppressed
progression
cell-based
xenograft
patient-derived
(PDX)
models.
Mechanistically,
transcriptionally
upregulated
by
nuclear
factor
T
3
(NFATc3),
translocated
nucleus
response
summary,
our
study
suggests
CPT-mediated
FA
combined
conventional
a
promising
strategy
for
patients
cancers.
Tumor Biology,
Journal Year:
2020,
Volume and Issue:
42(10), P. 101042832096528 - 101042832096528
Published: Oct. 1, 2020
Glucose,
as
the
main
consuming
nutrient
of
body,
faces
different
destinies
in
cancer
cells.
Glycolysis,
oxidative
phosphorylation,
and
pentose
phosphate
pathways
produce
glucose-derived
metabolites
thus
affect
cells’
bioenergetics
differently.
Tumor
dependency
to
aerobic
glycolysis
other
cancer-specific
metabolism
changes
are
known
hallmarks,
distinct
cells
from
normal
Therefore,
these
tumor-specific
characteristics
receive
limelight
targets
for
therapy.
Glutamine,
serine,
fatty
acid
oxidation
together
with
5-lipoxygenase
that
have
attracted
lots
attention
In
this
review,
we
not
only
discuss
tumor
aspects
but
also
roles
promotion
at
stages
their
difference
Besides,
dissect
inhibitors
potential
blocking
metabolic
introduce
effective
non-effective
field.
International Journal of Molecular Sciences,
Journal Year:
2020,
Volume and Issue:
21(9), P. 3100 - 3100
Published: April 28, 2020
Reactive
Oxygen
Species
or
“ROS”
encompass
several
molecules
derived
from
oxygen
that
can
oxidize
other
and
subsequently
transition
rapidly
between
species.
The
key
roles
of
ROS
in
biological
processes
are
cell
signaling,
biosynthetic
processes,
host
defense.
In
cancer
cells,
increased
production
oxidative
stress
instigated
by
carcinogens,
oncogenic
mutations,
importantly,
metabolic
reprograming
the
proliferating
cells.
Increased
activates
myriad
downstream
survival
pathways
further
progression
metastasis.
this
review,
we
highlight
relation
ROS,
programing
cancer,
stromal
immune
cells
with
emphasis
on
transcription
machinery
involved
redox
homeostasis,
malignant
phenotype.
We
also
shed
light
therapeutic
targeting
generating
as
investigate:
Orlistat,
Biguandes,
AICAR,
2
Deoxyglucose,
CPI-613,
Etomoxir.
Cell Death and Disease,
Journal Year:
2023,
Volume and Issue:
14(1)
Published: Jan. 21, 2023
Obesity
is
a
risk
factor
in
various
types
of
cancer,
including
breast
cancer.
The
disturbance
adipose
tissue
obesity
highly
correlates
with
cancer
progression
and
resistance
to
standard
treatments
such
as
chemo-
radio-therapies.
In
this
study,
syngeneic
mouse
model
triple-negative
(TNBC),
diet-induced
(DIO)
not
only
promoted
tumor
growth,
but
also
reduced
response
radiotherapy.
Serpine1
(Pai-1)
was
elevated
the
circulation
obese
mice
enriched
within
microenvironment.
vitro
co-culture
human
white
adipocytes-conditioned
medium
(hAd-CM)
TNBC
cells
potentiated
aggressive
phenotypes
radioresistance
cells.
Moreover,
inhibition
both
cell
autonomous
non-autonomous
SERPINE1
by
either
genetic
or
pharmacological
strategy
markedly
dampened
Mechanistically,
we
uncovered
previously
unrecognized
role
DNA
damage
response.
Ionizing
radiation-induced
double-strand
breaks
(DSBs)
increased
expression
an
ATM/ATR-dependent
manner,
nuclear
localization
facilitate
DSB
repair.
By
analyzing
public
clinical
datasets,
higher
correlated
patients'
BMI
well
poor
outcomes.
Elevated
were
observed
radioresistant
Collectively,
reveal
link
between
identify
be
crucial
mediating
obesity-associated
radioresistance.
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(5), P. 4954 - 4954
Published: March 4, 2023
Abnormal
energy
metabolism
is
a
characteristic
of
tumor
cells,
and
mitochondria
are
important
components
metabolic
reprogramming.
Mitochondria
have
gradually
received
the
attention
scientists
due
to
their
functions,
such
as
providing
chemical
energy,
producing
substrates
for
anabolism,
controlling
REDOX
calcium
homeostasis,
participating
in
regulation
transcription,
cell
death.
Based
on
concept
reprogramming
mitochondrial
metabolism,
range
drugs
been
developed
target
mitochondria.
In
this
review,
we
discuss
current
progress
summarized
corresponding
treatment
options.
Finally,
propose
inner
membrane
transporters
new
feasible
therapeutic
targets.
Cancer Communications,
Journal Year:
2019,
Volume and Issue:
39(1), P. 1 - 13
Published: Aug. 29, 2019
Abstract
In
the
past
decade,
remarkable
progress
has
been
made
in
reprogramming
terminally
differentiated
somatic
cells
and
cancer
into
induced
pluripotent
with
benign
phenotypes.
Recent
studies
have
explored
various
approaches
to
induce
from
one
cell
type
another,
including
lineage‐specific
transcription
factors‐,
combinatorial
small
molecules‐,
microRNAs‐
embryonic
microenvironment‐derived
exosome‐mediated
reprogramming.
These
proven
be
technically
feasible
versatile
enable
re‐activation
of
sequestered
epigenetic
regions,
thus
driving
fate
decisions
cells.
One
significant
utilities
is
therapeutic
potential
retrieving
normal
functions
malignancies.
However,
there
are
several
major
obstacles
overcome
before
clinical
translation,
characterization
mechanisms,
improvement
efficiency
safety,
development
delivery
methods.
Recently,
insights
mechanism
proposed,
determining
achieved
promote
feasibility,
allowing
it
emerge
as
a
promising
therapy
against
near
future.
This
review
aims
discuss
recent
applications
reprogramming,
focus
on
significance
limitations
different
approaches,
while
summarizing
vital
roles
played
by
factors,
molecules,
microRNAs
exosomes
during
process.
Cancers,
Journal Year:
2020,
Volume and Issue:
12(12), P. 3798 - 3798
Published: Dec. 16, 2020
Obesity
is
a
modern
health
problem
that
has
reached
pandemic
proportions.
It
an
established
risk
factor
for
carcinogenesis,
however,
evidence
the
contribution
of
adipose
tissue
to
metastatic
behavior
tumors
also
mounting.
Over
90%
cancer
mortality
attributed
metastasis
and
tumor
cells
must
communicate
with
their
microenvironment
survival.
Many
characteristics
observed
in
obese
strongly
mirror
microenvironment.
Thus
case
prostate,
pancreatic
breast
esophageal
adenocarcinoma,
which
are
all
located
close
anatomical
proximity
depot,
adjacent
fat
provides
ideal
enhance
growth,
progression
metastasis.
Adipocytes
provide
adipokines,
fatty
acids
other
soluble
factors
whilst
immune
infiltrate
In
addition,
there
emerging
studies
on
role
extracellular
vesicles
secreted
from
tissue,
matrix
itself,
as
drivers
obesity-induced
present
review,
we
discuss
major
mechanisms
responsible
obesity–metastatic
link.
Furthermore,
understanding
these
complex
will
novel
therapies
halt
tumor–adipose
crosstalk
ultimate
aim
inhibiting
growth.