Seminars in Cancer Biology,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Dec. 1, 2024
Elevated
lipid
metabolism
is
one
of
hallmarks
malignant
tumors.
Lipids
not
only
serve
as
essential
structural
components
biological
membranes
but
also
provide
energy
and
substrates
for
the
proliferation
cancer
cells
tumor
growth.
Cancer
meet
their
needs
by
coordinating
processes
absorption,
synthesis,
transport,
storage,
catabolism.
As
research
in
this
area
continues
to
deepen,
numerous
new
discoveries
have
emerged,
making
it
crucial
scientists
stay
informed
about
developments
metabolism.
In
review,
we
first
discuss
relevant
concepts
theories
or
assumptions
that
help
us
understand
-based
therapies.
We
then
systematically
summarize
latest
advancements
including
mechanisms,
novel
targets,
up-to-date
pre-clinical
clinical
investigations
anti-cancer
treatment
with
targeted
drugs.
Finally,
emphasize
emerging
directions
therapeutic
strategies,
future
prospective
challenges.
This
review
aims
insights
guidance
field
Scientific Reports,
Journal Year:
2025,
Volume and Issue:
15(1)
Published: Jan. 8, 2025
Mendelian
randomization
(MR)
was
employed
to
investigate
the
causal
relationships
between
immune
cell
phenotypes,
hyperthyroidism
(HD),
and
potential
metabolic
mediators.
In
this
study,
we
acquired
731
phenotypes
from
genome-wide
association
studies
(GWAS)
(n
=
18,622),
HD
data
research
by
Handan
Melike
Dönertaş
et
al.
(3,731
cases,
480,867
controls),
aggregated
statistics
of
1,400
blood
metabolites
UK
Biobank
115,078).
Bidirectional
MR
analysis
performed
explore
HD,
two-sample
multi-variable
were
conducted
identify
plasma
mediating
in
HD.
addition,
sensitivity
analyses
used
evaluate
robustness,
heterogeneity,
horizontal
pleiotropy
results.
Single-cell
transcriptome-based
exploration
key
molecule
mechanism
which
regulated
differentiation
pathogenesis.
Co-localization
using
single-cell
eQTL
(sc-eQTL)
with
probe
genetically
shared
effects.
Two-sample
MRshowed
that
CD25
on
naive-mature
B
cell,
CD8
+
NKT
thymol
sulfate
level
found
have
(P
<
0.008).
The
relationship
further
validated
an
independent
cohort
inverse-variance
weighted
(IVW).
cells
both
negatively
correlated
0.05).
results
remained
significant
after
MR-Egger
MR-PRESSO
correction
for
heterogeneity
>
Multi-variable
showed
mediated
8.67%
10.4%
associations
respectively.
Moreover,
evolution
microenvironment,
identifying
PTPRC,
PTK2B,
KDM5A
TIGIT
as
participating
molecules.
molecules
had
genetic
sharing
effects
(PPH4
0.75,
R2
0.8,
P
0.05),
PTK2B
having
broadest
interval.
Current
study
provides
evidence
supporting
several
specific
well
metabolites.
Thymol
may
increases
risk
pathogenesis
variants
inducing
progression
microenvironment.
Livers,
Journal Year:
2025,
Volume and Issue:
5(1), P. 5 - 5
Published: Jan. 27, 2025
Liver
fibrosis
is
a
very
complicated
dynamic
process
where
several
immune
cells
are
involved.
Both
innate
and
adaptive
immunity
implicated,
their
interplay
always
present.
Multi-directional
interactions
between
liver
macrophages,
hepatic
stellate
(HSCs),
cells,
cytokines
important
for
the
induction
perpetuation
of
fibrosis.
Detailed
studies
proteomics
transcriptomics
have
produced
new
evidence
role
individual
in
cirrhosis.
Most
these
controlled
by
various
checkpoints
whose
main
function
to
maintain
homeostasis
implicated
cells.
Recent
indicates
that
involved
In
particular,
programmed
cell
death
protein
1
(PD-1),
death-ligand
(PD-L1),
cytotoxic
T
lymphocyte-associated
antigen
4
(CTLA-4)
been
investigated,
particularly
after
availability
checkpoint
inhibitors.
Their
activation
leads
exhaustion
CD4+ve
CD8+ve
promotion
this
review,
current
pathogenesis
immunological
abnormalities
discussed.
The
recent
data
on
involvement
identified
as
possible
targets
future
interventions.
Frontiers in Immunology,
Journal Year:
2025,
Volume and Issue:
16
Published: Feb. 14, 2025
Metabolic
reprogramming
is
one
of
the
major
biological
features
malignant
tumors,
playing
a
crucial
role
in
initiation
and
progression
cancer.
The
tumor
microenvironment
consists
various
non-cancer
cells,
such
as
hepatic
stellate
cancer-associated
fibroblasts
(CAFs),
immune
well
extracellular
matrix
soluble
substances.
In
liver
cancer,
metabolic
not
only
affects
its
own
growth
survival
but
also
interacts
with
other
cells
by
influencing
expression
release
metabolites
cytokines
(such
lactate,
PGE2,
arginine).
This
interaction
leads
to
acidification
restricts
uptake
nutrients
resulting
competition
symbiosis.
At
same
time,
neighboring
during
proliferation
differentiation
processes
impacts
immunity.
article
provides
comprehensive
overview
crosstalk
between
cancer
their
microenvironment,
deepening
our
understanding
relevant
findings
pathways.
contributes
further
regulation
development
evasion
mechanisms
while
providing
assistance
advancing
personalized
therapies
targeting
pathways
for
anti-cancer
treatment.
Bioscience Reports,
Journal Year:
2023,
Volume and Issue:
43(1)
Published: Jan. 1, 2023
Abstract
Hepatocellular
carcinoma
(HCC)
is
the
fourth
leading
cause
of
cancer-related
death
worldwide.
In
recent
years
nonalcoholic
fatty
liver
disease
(NAFLD)
becoming
a
growing
HCCs
and
incidence
NAFLD-related
expected
to
further
dramatically
increase
by
next
decade.
Chronic
inflammation
regarded
as
driving
force
NAFLD
progression
key
factor
in
hepatic
carcinogenesis.
Hepatic
results
from
persistent
stimulation
innate
immunity
response
hepatocellular
injury
gut
dysbiosis
well
activation
adaptive
immunity.
However,
relative
roles
processes
HCC
are
still
incompletely
characterized.
This
due
complex
interplay
between
different
cell
populations,
which
also
strongly
influenced
gut-derived
bacterial
products,
metabolic/nutritional
signals.
Furthermore,
carcinogenic
mechanisms
NAFLD/NASH
appear
involve
signals
mediated
hypoxia
inducible
factors.
review
discusses
data
regarding
contribution
inflammatory
cells
their
possible
impact
on
patient
current
treatments.
International Journal of Biological Sciences,
Journal Year:
2024,
Volume and Issue:
20(6), P. 2044 - 2071
Published: Jan. 1, 2024
Cholesterol
is
crucial
for
cell
survival
and
growth,
dysregulation
of
cholesterol
homeostasis
has
been
linked
to
the
development
cancer.
The
tumor
microenvironment
(TME)
facilitates
crosstalk
between
metabolism
TME
contributes
tumorigenesis
progression.
Targeting
demonstrated
significant
antitumor
effects
in
preclinical
clinical
studies.
In
this
review,
we
discuss
regulatory
mechanisms
impact
its
on
hallmarks
We
also
describe
how
reprograms
across
seven
specialized
microenvironments.
Furthermore,
potential
targeting
as
a
therapeutic
strategy
tumors.
This
approach
not
only
exerts
monotherapy
combination
therapy
but
mitigates
adverse
associated
with
conventional
therapy.
Finally,
outline
unresolved
questions
suggest
avenues
future
investigations
relation
Cell Death and Disease,
Journal Year:
2024,
Volume and Issue:
15(5)
Published: May 9, 2024
Cholesterol
metabolism
reprogramming
is
one
of
the
significant
characteristics
hepatocellular
carcinoma
(HCC).
increases
risk
epithelial-mesenchymal
transition
(EMT)
in
cancer.
Sterol
O-acyltransferases
1
(SOAT1)
maintains
cholesterol
homeostasis.
However,
exact
mechanistic
contribution
SOAT1
to
EMT
HCC
remains
unclear.
Here
we
demonstrated
that
positively
related
poor
prognosis
HCC,
markers
and
promoted
cell
migration
invasion
vitro,
which
was
mediated
by
increased
plasmalemma
esters
accumulation.
Furthermore,
reported
disrupted
homeostasis
accelerate
tumorigenesis
development
xenograft
NAFLD-HCC.
Also,
detected
nootkatone,
a
sesquiterpene
ketone,
inhibited
targeting
vitro
vivo.
Collectively,
our
finding
indicated
promotes
contributes
hepatocarcinogenesis
increasing
esterification,
suppressed
efficiently
nootkatone.
This
study
potential
biomarker
therapeutic
target
NAFLD-HCC
SOAT1-targeting
inhibitors
are
expected
be
new
treatment
for
HCC.
Journal of Hepatocellular Carcinoma,
Journal Year:
2024,
Volume and Issue:
Volume 11, P. 327 - 346
Published: Feb. 1, 2024
Abstract:
Hepatocellular
carcinoma
(HCC)
stands
as
a
severe
malignant
tumor
with
profound
impact
on
overall
health,
often
accompanied
by
an
unfavorable
prognosis.
Despite
some
advancements
in
the
diagnosis
and
treatment
of
this
disease,
improving
prognosis
HCC
remains
formidable
challenge.
It
is
noteworthy
that
lipid
metabolism
plays
pivotal
role
onset,
development,
progression
cells.
Existing
research
indicates
potential
application
targeting
HCC.
This
review
aims
to
thoroughly
explore
alterations
HCC,
offering
detailed
account
advantages
associated
innovative
therapeutic
strategies
metabolism.
Targeting
holds
promise
for
potentially
enhancing
Keywords:
cholesterol,
fatty
acid,
hepatocellular
carcinoma,
uptake,
catabolism,
synthesis