Frontiers in Oncology,
Journal Year:
2019,
Volume and Issue:
9
Published: Nov. 15, 2019
Metabolism
encompasses
the
biochemical
processes
that
allow
healthy
cells
to
keep
energy,
redox
balance
and
building
blocks
required
for
cell
development,
survival,
proliferation
steady.
Malignant
are
well-documented
reprogram
their
metabolism
energy
production
networks
support
rapid
survival
in
harsh
conditions
via
mutations
oncogenes
inactivation
of
tumor
suppressor
genes.
Despite
histologic
genetic
heterogeneity
tumors,
a
common
set
metabolic
pathways
sustain
high
rates
observed
cancer
cells.
This
review
with
focus
on
lung
covers
several
fundamental
principles
disturbed
glucose
metabolism,
such
as
"Warburg"
effect,
importance
glycolysis
its
branching
pathways,
unanticipated
gluconeogenesis
mitochondrial
metabolism.
Furthermore,
we
highlight
our
current
understanding
how
this
might
result
development
new
treatments.
Cells,
Journal Year:
2021,
Volume and Issue:
10(5), P. 1056 - 1056
Published: April 29, 2021
Cancer
cells
alter
metabolic
processes
to
sustain
their
characteristic
uncontrolled
growth
and
proliferation.
These
alterations
include
(1)
a
shift
from
oxidative
phosphorylation
aerobic
glycolysis
support
the
increased
need
for
ATP,
(2)
glutaminolysis
NADPH
regeneration,
(3)
altered
flux
through
pentose
phosphate
pathway
tricarboxylic
acid
cycle
macromolecule
generation,
(4)
lipid
uptake,
lipogenesis,
cholesterol
synthesis,
(5)
upregulation
of
one-carbon
metabolism
production
NADH/NADPH,
nucleotides,
glutathione,
(6)
amino
metabolism,
(7)
metabolism-based
regulation
apoptosis,
(8)
utilization
alternative
substrates,
such
as
lactate
acetate.
Altered
in
cancer
is
controlled
by
tumor-host
cell
interactions,
key
oncogenes,
tumor
suppressors,
other
regulatory
molecules,
including
non-coding
RNAs.
Changes
pathways
are
dynamic,
exhibit
plasticity,
often
dependent
on
type
microenvironment,
leading
thought
Warburg
Effect
"reverse
Effect"
plasticity.
Understanding
complex
nature
these
multiple
can
development
new
therapies.
Signal Transduction and Targeted Therapy,
Journal Year:
2020,
Volume and Issue:
5(1)
Published: Oct. 7, 2020
Abstract
Nicotinamide
adenine
dinucleotide
phosphate
(NADPH)
is
an
essential
electron
donor
in
all
organisms,
and
provides
the
reducing
power
for
anabolic
reactions
redox
balance.
NADPH
homeostasis
regulated
by
varied
signaling
pathways
several
metabolic
enzymes
that
undergo
adaptive
alteration
cancer
cells.
The
reprogramming
of
renders
cells
both
highly
dependent
on
this
network
antioxidant
capacity
more
susceptible
to
oxidative
stress.
Modulating
unique
might
be
effective
strategy
eliminate
these
In
review,
we
summarize
current
existing
literatures
homeostasis,
including
its
biological
functions,
regulatory
mechanisms
corresponding
therapeutic
interventions
human
cancers,
providing
insights
into
implications
targeting
metabolism
associated
mechanism
therapy.
Genes & Development,
Journal Year:
2021,
Volume and Issue:
35(11-12), P. 787 - 820
Published: June 1, 2021
Colorectal
cancer
has
served
as
a
genetic
and
biological
paradigm
for
the
evolution
of
solid
tumors,
these
insights
have
illuminated
early
detection,
risk
stratification,
prevention,
treatment
principles.
Employing
hallmarks
framework,
we
provide
conceptual
framework
to
understand
how
alterations
in
colorectal
drive
cell
biology
properties
shape
heterotypic
interactions
across
cells
tumor
microenvironment.
This
review
details
research
advances
pertaining
genetics
cancer,
emerging
concepts
gleaned
from
immune
single-cell
profiling,
critical
remaining
knowledge
gaps
influencing
development
effective
therapies
this
that
remains
major
public
health
burden.
Frontiers in Immunology,
Journal Year:
2018,
Volume and Issue:
9
Published: July 30, 2018
Unrestricted
cell
proliferation
is
a
hallmark
of
cancer.
Purines
are
basic
components
nucleotides
in
proliferation,
thus
impaired
purine
metabolism
associated
with
the
progression
The
de
novo
biosynthesis
depends
on
six
enzymes
to
catalyze
conversion
phosphoribosylpyrophosphate
inosine
5'-monophosphate.
These
cluster
around
mitochondria
and
microtubules
form
purinosome,
which
multi-enzyme
complex
involved
requirement.
In
this
review,
we
highlighted
purinosome
biology
emphasis
therapeutic
potential
manipulating
or
cancers.
We
also
reviewed
current
advances
our
understanding
mammalian
target
rapamycin
(mTOR)
for
regulating
formation
cancers,
discussed
future
prospects
targeting
treat
Frontiers in Cell and Developmental Biology,
Journal Year:
2021,
Volume and Issue:
8
Published: Jan. 12, 2021
Metabolic
reprogramming
has
been
widely
recognized
as
a
hallmark
of
malignancy.
The
uptake
and
metabolism
amino
acids
are
aberrantly
upregulated
in
many
cancers
that
display
addiction
to
particular
acids.
Amino
facilitate
the
survival
proliferation
cancer
cells
under
genotoxic,
oxidative,
nutritional
stress.
Thus,
targeting
acid
is
becoming
potential
therapeutic
strategy
for
patients.
In
this
review,
we
will
systematically
summarize
recent
progress
malignancy
discuss
their
interconnection
with
mammalian
target
rapamycin
complex
1
(mTORC1)
signaling,
epigenetic
modification,
tumor
growth
immunity,
ferroptosis.
Finally,
highlight
applications.
Cancers,
Journal Year:
2019,
Volume and Issue:
11(5), P. 675 - 675
Published: May 15, 2019
Far
beyond
simply
being
11
of
the
20
amino
acids
needed
for
protein
synthesis,
non-essential
play
numerous
important
roles
in
tumor
metabolism.
These
diverse
functions
include
providing
precursors
biosynthesis
macromolecules,
controlling
redox
status
and
antioxidant
systems,
serving
as
substrates
post-translational
epigenetic
modifications.
This
functional
diversity
has
sparked
great
interest
targeting
acid
metabolism
cancer
therapy
motivated
development
several
therapies
that
are
either
already
used
clinic
or
currently
clinical
trials.
In
this
review,
we
will
discuss
each
cancer,
how
their
metabolic
pathways
linked,
researchers
working
to
overcome
unique
challenges
therapy.
