Cancers,
Journal Year:
2025,
Volume and Issue:
17(7), P. 1094 - 1094
Published: March 25, 2025
Oral
cancer
refers
to
cancers
originating
in
the
oral
cavity
and
oropharyngeal
regions.
It
is
16th
most
prevalent
sixth
leading
cause
of
cancer-related
deaths.
However,
mechanisms
its
progression
are
still
being
understood,
interventions
provide
early
diagnosis
need
be
improved.
More
studies
have
recently
been
conducted
on
cancer,
many
reviews
summarized
findings
this
field,
focusing
individual
factors.
few
review
articles
evaluated
combinational
impacts
different
factors
cancer.
This
aimed
an
overview
effects
three
extracellular
factors,
including
lifestyle
habits,
microbiome,
socioeconomic
progression.
differentially
affected
by
habits;
high-sugar
diets,
processed
foods,
alcohol,
smoking,
possibly
sleep
disorders
benefit
progression,
whereas
eating
natural
such
as
fruits,
vegetables,
fish,
garlic,
drinking
tea
or
coffee,
physical
exercise
can
combat
it.
The
microbiome
could
suppress
promote
Low
status
impact
development.
Furthermore,
crosstalk
among
these
affects
has
limitations
not
all
cancer-affecting
important
publications.
focus
should
placed
multiple
treatment.
study
update
researchers
landscape
help
formulate
approaches
prevention
Cancer and Metastasis Reviews,
Journal Year:
2024,
Volume and Issue:
43(3), P. 1095 - 1116
Published: April 11, 2024
Abstract
Tumor
microenvironment
(TME)
has
been
demonstrated
to
play
a
significant
role
in
tumor
initiation,
progression,
and
metastasis.
Cancer-associated
fibroblasts
(CAFs)
are
the
major
component
of
TME
exhibit
heterogeneous
properties
their
communication
with
cells.
This
heterogeneity
CAFs
can
be
attributed
various
origins,
including
quiescent
fibroblasts,
mesenchymal
stem
cells
(MSCs),
adipocytes,
pericytes,
endothelial
cells,
mesothelial
Moreover,
single-cell
RNA
sequencing
identified
diverse
phenotypes
CAFs,
myofibroblastic
(myCAFs)
inflammatory
(iCAFs)
being
most
acknowledged,
alongside
newly
discovered
subtypes
like
antigen-presenting
(apCAFs).
Due
these
heterogeneities,
exert
multiple
functions
tumorigenesis,
cancer
stemness,
angiogenesis,
immunosuppression,
metabolism,
As
result,
targeted
therapies
aimed
at
TME,
particularly
focusing
on
rapidly
developing,
fueling
promising
future
advanced
tumor-targeted
therapy.
Clinical and Translational Medicine,
Journal Year:
2024,
Volume and Issue:
14(3)
Published: March 1, 2024
Abstract
Heightened
lactate
production
in
cancer
cells
has
been
linked
to
various
cellular
mechanisms
such
as
angiogenesis,
hypoxia,
macrophage
polarisation
and
T‐cell
dysfunction.
The
lactate‐induced
lactylation
of
histone
lysine
residues
is
noteworthy,
it
functions
an
epigenetic
modification
that
directly
augments
gene
transcription
from
chromatin.
This
originating
effectively
fosters
a
reliance
on
transcription,
thereby
expediting
tumour
progression
development.
Herein,
this
review
explores
the
correlation
between
characteristics,
revealing
innovative
process
enhances
vulnerability
malignancy.
Moreover,
imperative
acknowledge
paramount
importance
acknowledging
therapeutic
methodologies
for
proficiently
managing
by
precisely
targeting
signalling.
comprehensive
illuminates
crucial
yet
inadequately
investigated
aspect
lactylation,
providing
valuable
insights
into
its
clinical
ramifications
prospective
interventions
centred
lactylation.
Abstract
Hypoxia-inducible
factors
(HIFs)
are
essential
transcription
that
orchestrate
cellular
responses
to
oxygen
deprivation.
HIF-1α,
as
an
unstable
subunit
of
HIF-1,
is
usually
hydroxylated
by
prolyl
hydroxylase
domain
enzymes
under
normoxic
conditions,
leading
ubiquitination
and
proteasomal
degradation,
thereby
keeping
low
levels.
Instead
hypoxia,
sometimes
even
in
normoxia,
HIF-1α
translocates
into
the
nucleus,
dimerizes
with
HIF-1β
generate
then
activates
genes
involved
adaptive
such
angiogenesis,
metabolic
reprogramming,
survival,
which
presents
new
challenges
insights
its
role
processes.
Thus,
review
delves
mechanisms
HIF-1
maintains
stability
normoxia
including
but
not
limited
giving
transcriptional,
translational,
well
posttranslational
regulation
underscore
pivotal
adaptation
malignancy.
Moreover,
extensively
cancer
cardiovascular
diseases
potentially
serves
a
bridge
between
them.
An
overview
HIF-1-related
drugs
approved
or
clinical
trials
summarized,
highlighting
their
potential
capacity
for
targeting
toxicity
related
treatment.
The
provides
comprehensive
insight
HIF-1’s
regulatory
mechanism
paves
way
future
research
therapeutic
development.
Molecular Aspects of Medicine,
Journal Year:
2025,
Volume and Issue:
101, P. 101335 - 101335
Published: Jan. 1, 2025
Renal
cell
carcinoma
(RCC)
is
a
malignant
tumor
with
highly
heterogeneous
and
complex
molecular
mechanisms.
Through
systematic
analysis
of
TCGA,
COSMIC
other
databases,
24
mutated
genes
closely
related
to
RCC
were
screened,
including
VHL,
PBRM1,
BAP1
SETD2,
which
play
key
roles
in
signaling
pathway
transduction,
chromatin
remodeling
DNA
repair.
The
PI3K/AKT/mTOR
particularly
important
the
pathogenesis
RCC.
Mutations
such
as
PIK3CA,
MTOR
PTEN
are
associated
metabolic
abnormalities
proliferation.
Clinically,
mTOR
inhibitors
VEGF-targeted
drugs
have
shown
significant
efficacy
personalized
therapy.
Abnormal
regulation
reprogramming,
especially
glycolysis
glutamine
pathways,
provides
cells
continuous
energy
supply
survival
advantages,
GLS1
promising
results
preclinical
studies.
This
paper
also
explores
potential
immune
checkpoint
combination
targeted
drugs,
well
application
nanotechnology
drug
delivery
In
addition,
unique
mechanisms
revealed
individualized
therapeutic
strategies
explored
for
specific
subtypes
TFE3,
TFEB
rearrangement
type
SDHB
mutant
type.
review
summarizes
common
gene
mutations
their
mechanisms,
emphasizes
diagnosis,
treatment
prognosis,
looks
forward
prospects
multi-pathway
therapy,
immunotherapy
treatment,
providing
theoretical
support
clinical
guidance
new
development.
Cell Communication and Signaling,
Journal Year:
2024,
Volume and Issue:
22(1)
Published: Jan. 12, 2024
Abstract
Objective
The
CD155/TIGIT
axis
has
attracted
considerable
interest
as
an
emerging
immune
checkpoint
with
potential
applications
in
cancer
immunotherapy.
Our
research
focused
on
investigating
the
role
of
checkpoints
progression
triple-negative
breast
(TNBC).
Methods
We
evaluated
CD155
and
TIGIT
expression
TNBC
tissues
using
both
immunohistochemistry
(IHC)
gene
profiling.
experiments,
vivo
vitro,
provided
evidence
that
inhibiting
pathway
reinstates
ability
CD8
+
T
cells
to
generate
cytokines.
To
assess
impact
signaling
blockade,
we
utilized
Glucose
Assay
Kits
Lactate
measure
alterations
glucose
lactate
levels
within
cells.
employed
western
blotting
(WB)
investigate
glycolytic-related
proteins
PI3K/AKT/mTOR
pathways
following
inhibition
signaling.
Results
exhibits
heightened
a
negative
correlation
extent
infiltrating
Furthermore,
patients
demonstrate
elevated
expression.
findings
indicate
interaction
between
disrupts
metabolism
by
suppressing
activation
pathway,
ultimately
leading
reduced
production
cytokines
Both
vitro
experiments
have
conclusively
demonstrated
capacity
Moreover,
administration
blocking
antibody
against
not
only
inhibits
tumor
growth
but
also
augments
functionality
lymphocytes.
Conclusions
strongly
suggest
represents
promising
therapeutic
target
for
treating
TNBC.
Frontiers in Bioscience-Landmark,
Journal Year:
2024,
Volume and Issue:
29(3)
Published: March 13, 2024
Altered
metabolism
represents
a
fundamental
difference
between
cancer
cells
and
normal
cells.
Cancer
have
unique
ability
to
reprogram
their
by
deviating
reliance
from
primarily
oxidative
phosphorylation
(OXPHOS)
glycolysis,
in
order
support
survival.
This
metabolic
phenotype
is
referred
as
the
“Warburg
effect”
associated
with
an
increase
glucose
uptake,
diversion
of
glycolytic
intermediates
alternative
pathways
that
anabolic
processes.
These
processes
include
synthesis
nucleic
acids,
lipids,
proteins,
necessary
for
rapidly
dividing
cells,
sustaining
growth,
proliferation,
capacity
successful
metastasis.
Triple-negative
breast
(TNBC)
one
most
aggressive
subtypes
cancer,
poorest
patient
outcome
due
its
high
rate
TNBC
characterized
elevated
glycolysis
certain
instances,
low
OXPHOS.
dysregulation
linked
chemotherapeutic
resistance
research
models
samples.
There
more
than
single
mechanism
which
this
switch
occurs
here,
we
review
current
knowledge
relevant
molecular
mechanisms
involved
advanced
metabolism,
focusing
on
TNBC.
Warburg
effect,
adaptations,
microRNA
regulation,
mitochondrial
involvement,
calcium
signaling,
recent
player
JAK/STAT
signaling.
In
addition,
explore
some
drugs
compounds
targeting
reprogramming.
Research
these
highly
promising
could
ultimately
offer
new
opportunities
development
innovative
therapies
treat
dysregulated
metabolism.
Journal of Translational Medicine,
Journal Year:
2025,
Volume and Issue:
23(1)
Published: March 6, 2025
Gastric
cancer
(GC)
is
one
of
the
most
common
malignancies.
Previous
studies
have
shown
that
mitochondrial
metabolism
associated
with
However,
relevant
research
on
mitochondria-related
lncRNAs
in
GC
lacking.
We
integrated
corresponding
information
patients
from
The
Cancer
Genome
Atlas
(TCGA)
database.
Mitochondria-related
were
selected
based
differential
expression
and
a
correlation
analysis
to
construct
prognostic
model.
mutation
data
analyzed
distinguish
differences
tumor
burden
(TMB).
Single-sample
gene
set
enrichment
(ssGSEA)
was
performed
evaluate
immunological
differences.
A
series
cell-based
experiments
adopted
biological
behavior
GC.
total
1571
identified.
signature
incorporating
nine
built
293
suitable
cases
could
predict
patient
prognosis.
TMB
ssGSEA
indicated
low-risk
group
displayed
increased
immune
function.
differentially
expressed
genes
enriched
metabolic
functions.
AC129507.1
significantly
upregulated
cells
poor
prognosis,
its
knockdown
inhibited
proliferation
migration
cells.
Mechanistically,
silencing
led
abnormal
glycolipid
oxidative
stress,
thus
inducing
ferroptosis.
Our
nine-lncRNA
risk
powerfully
promoted
malignant
phenotypes
play
nonnegligible
role
by
promoting
formation
immunosuppressive
microenvironment
inhibiting
initiation
ferroptosis,
which
needs
be
further
explored.