MedComm,
Journal Year:
2025,
Volume and Issue:
6(3)
Published: March 1, 2025
The
rising
trend
in
global
cancer
incidence
has
caused
widespread
concern,
one
of
the
main
reasons
being
aging
population.
Statistical
data
show
that
and
mortality
rates
a
clear
upward
with
age.
Although
there
is
commonality
between
dysregulated
nutrient
sensing,
which
features
aging,
metabolic
reprogramming
tumor
cells,
specific
regulatory
relationship
not
clear.
This
manuscript
intends
to
comprehensively
analyze
senescence
reprogramming;
as
well
reveal
impact
key
factors
leading
cellular
on
tumorigenesis.
In
addition,
this
review
summarizes
current
intervention
strategies
targeting
sensing
pathways,
clinical
cases
treating
tumors
characteristics
existing
nanodelivery
research
strategies.
Finally,
it
also
suggests
sensible
dietary
habits
for
those
who
wish
combat
aging.
conclusion,
attempts
sort
out
link
metabolism
provide
new
ideas
treatment.
Journal of Hematology & Oncology,
Journal Year:
2023,
Volume and Issue:
16(1)
Published: June 26, 2023
Abstract
Exosomal
circRNA
serves
a
novel
genetic
information
molecule,
facilitating
communication
between
tumor
cells
and
microenvironmental
cells,
such
as
immune
fibroblasts,
other
components,
thereby
regulating
critical
aspects
of
cancer
progression
including
escape,
angiogenesis,
metabolism,
drug
resistance,
proliferation
metastasis.
Interestingly,
microenvironment
have
new
findings
in
influencing
escape
mediated
by
the
release
exosomal
circRNA.
Given
intrinsic
stability,
abundance,
broad
distribution
circRNAs,
they
represent
excellent
diagnostic
prognostic
biomarkers
for
liquid
biopsy.
Moreover,
artificially
synthesized
circRNAs
may
open
up
possibilities
therapy,
potentially
bolstered
nanoparticles
or
plant
exosome
delivery
strategies.
In
this
review,
we
summarize
functions
underlying
mechanisms
cell
non-tumor
cell-derived
progression,
with
special
focus
on
their
roles
immunity
metabolism.
Finally,
examine
potential
application
therapeutic
targets,
highlighting
promise
clinical
use.
Signal Transduction and Targeted Therapy,
Journal Year:
2024,
Volume and Issue:
9(1)
Published: May 27, 2024
Notch
signaling,
renowned
for
its
role
in
regulating
cell
fate,
organ
development,
and
tissue
homeostasis
across
metazoans,
is
highly
conserved
throughout
evolution.
The
receptor
ligands
are
transmembrane
proteins
containing
epidermal
growth
factor-like
repeat
sequences,
typically
necessitating
receptor-ligand
interaction
to
initiate
classical
signaling
transduction.
Accumulating
evidence
indicates
that
the
pathway
serves
as
both
an
oncogenic
factor
a
tumor
suppressor
various
cancer
types.
Dysregulation
of
this
promotes
epithelial-mesenchymal
transition
angiogenesis
malignancies,
closely
linked
proliferation,
invasion,
metastasis.
Furthermore,
contributes
maintaining
stem-like
properties
cells,
thereby
enhancing
invasiveness.
regulatory
metabolic
reprogramming
microenvironment
suggests
pivotal
involvement
balancing
suppressive
effects.
Moreover,
implicated
conferring
chemoresistance
cells.
Therefore,
comprehensive
understanding
these
biological
processes
crucial
developing
innovative
therapeutic
strategies
targeting
signaling.
This
review
focuses
on
research
progress
cancers,
providing
in-depth
insights
into
potential
mechanisms
regulation
occurrence
progression
cancer.
Additionally,
summarizes
pharmaceutical
clinical
trials
therapy,
aiming
offer
new
human
malignancies.
Signal Transduction and Targeted Therapy,
Journal Year:
2024,
Volume and Issue:
9(1)
Published: Oct. 9, 2024
Metabolism,
including
glycolysis,
oxidative
phosphorylation,
fatty
acid
oxidation,
and
other
metabolic
pathways,
impacts
the
phenotypes
functions
of
immune
cells.
The
regulation
system
is
important
in
pathogenesis
progression
numerous
diseases,
such
as
cancers,
autoimmune
diseases
diseases.
concept
immunometabolism
was
introduced
over
a
decade
ago
to
elucidate
intricate
interplay
between
metabolism
immunity.
definition
has
expanded
from
chronic
low-grade
inflammation
reprogramming
cells
various
With
being
proposed
developed,
can
be
gradually
summarized
becomes
more
clearer.
In
context
many
cancer,
disease,
occurs
inducing
proinflammatory
or
anti-inflammatory
effects.
phenotypic
functional
changes
caused
by
further
affect
development
Based
on
experimental
results,
targeting
cellular
promising
therapy.
this
review,
we
focus
introduce
their
pathways
reprogramming,
summarize
how
these
effects
We
thoroughly
explore
targets
treatments
based
existing
studies.
challenges
translating
results
into
clinical
applications
field
are
also
summarized.
believe
that
better
understanding
health
will
improve
management
most
Molecular Cancer,
Journal Year:
2024,
Volume and Issue:
23(1)
Published: Aug. 30, 2024
Drug
resistance
in
cancer
cells
significantly
diminishes
treatment
efficacy,
leading
to
recurrence
and
metastasis.
A
critical
factor
contributing
this
is
the
epigenetic
alteration
of
gene
expression
via
RNA
modifications,
such
as
N6-methyladenosine
(m6A),
N1-methyladenosine
(m1A),
5-methylcytosine
(m5C),
7-methylguanosine
(m7G),
pseudouridine
(Ψ),
adenosine-to-inosine
(A-to-I)
editing.
These
modifications
are
pivotal
regulating
splicing,
translation,
transport,
degradation,
stability.
Governed
by
"writers,"
"readers,"
"erasers,"
impact
numerous
biological
processes
progression,
including
cell
proliferation,
stemness,
autophagy,
invasion,
apoptosis.
Aberrant
can
lead
drug
adverse
outcomes
various
cancers.
Thus,
targeting
modification
regulators
offers
a
promising
strategy
for
overcoming
enhancing
efficacy.
This
review
consolidates
recent
research
on
role
prevalent
resistance,
with
focus
m6A,
m1A,
m5C,
m7G,
Ψ,
A-to-I
Additionally,
it
examines
regulatory
mechanisms
linked
underscores
existing
limitations
field.
Journal of Cancer,
Journal Year:
2023,
Volume and Issue:
14(13), P. 2574 - 2584
Published: Jan. 1, 2023
Background
and
aim:As
non-coding
RNAs,
circular
RNAs
(circRNAs)
contribute
to
the
progression
of
malignancies
by
regulating
various
biological
processes.In
prostate
cancer,
however,
there
is
still
a
lack
understanding
regarding
potential
molecular
pathways
roles
circRNAs.Methods:
Loss-off
function
experiments
were
performed
investigate
circRNA
in
cancer.Western
blot,
qRT-PCR,
IHC
assay
used
examine
expression
level
different
genes
or
circRNAs.Further
biology
conducted
uncover
mechanism
underlying
cancer
using
dual
luciferase
reporter
RNA
immunoprecipitation
(RIP)
assays.Results:
A
novel
(hsa_circ_0124696,
named
circROBO1)
was
identified
as
significantly
upregulated
both
cells
tissues.Suppression
circROBO1
attenuated
proliferation
cells.In
addition,
we
found
that
knockdown
remarkably
increased
sensitivity
enzalutamide
treatment.A
deceleration
glycolysis
rate
observed
after
inhibition
circROBO1,
which
could
suppress
growth
overcome
resistance
enzalutamide.Our
results
revealed
promotes
via
accelerating
glycolysis.
Conclusion:Our
study
role
circROBO1-miR-556-5p-PGK1
axis
therapeutic
target
cancer.
Molecular Cancer,
Journal Year:
2024,
Volume and Issue:
23(1)
Published: Aug. 27, 2024
Abstract
The
development
of
drug
resistance
remains
a
major
challenge
in
cancer
treatment.
Ferroptosis,
unique
type
regulated
cell
death,
plays
pivotal
role
inhibiting
tumour
growth,
presenting
new
opportunities
treating
chemotherapeutic
resistance.
Accumulating
studies
indicate
that
epigenetic
modifications
by
non-coding
RNAs
(ncRNA)
can
determine
vulnerability
to
ferroptosis.
In
this
review,
we
first
summarize
the
growth/development.
Then,
core
molecular
mechanisms
ferroptosis,
its
upstream
regulation,
and
downstream
effects
on
Finally,
review
recent
advances
understanding
how
ncRNAs
regulate
ferroptosis
from
such
modulate
This
aims
enhance
general
ncRNA-mediated
regulatory
which
highlighting
ncRNA-ferroptosis
axis
as
key
druggable
target
overcoming
MedComm,
Journal Year:
2024,
Volume and Issue:
5(9)
Published: Sept. 1, 2024
Abstract
Cell
death
regulation
is
essential
for
tissue
homeostasis
and
its
dysregulation
often
underlies
cancer
development.
Understanding
the
different
pathways
of
cell
can
provide
novel
therapeutic
strategies
battling
cancer.
This
review
explores
several
key
mechanisms
apoptosis,
necroptosis,
autophagic
death,
ferroptosis,
pyroptosis.
The
research
gap
addressed
involves
a
thorough
analysis
how
these
be
precisely
targeted
therapy,
considering
tumor
heterogeneity
adaptation.
It
delves
into
genetic
epigenetic
factors
signaling
cascades
like
phosphatidylinositol
3‐kinase/protein
kinase
B/mammalian
target
rapamycin
(PI3K/AKT/mTOR)
mitogen‐activated
protein
kinase/extracellular
signal‐regulated
(MAPK/ERK)
pathways,
which
are
critical
death.
Additionally,
interaction
microenvironment
with
cells,
particularly
influence
hypoxia,
nutrient
deprivation,
immune
cellular
interactions,
explored.
Emphasizing
strategies,
this
highlights
emerging
modulators
inducers
such
as
B
lymphoma
2
(BCL2)
homology
domain
3
(BH3)
mimetics,
tumour
necrosis
factor‐related
apoptosis‐inducing
ligand
(TRAIL),
chloroquine,
innovative
approaches
to
induce
ferroptosis
provides
insights
therapy's
future
direction,
focusing
on
multifaceted
circumvent
drug
resistance.
examination
evolving
underlines
considerable
clinical
potential
continuous
necessity
in‐depth
exploration
within
scientific
domain.
Drug Resistance Updates,
Journal Year:
2025,
Volume and Issue:
81, P. 101226 - 101226
Published: March 3, 2025
TRAP1
is
involved
in
metabolic
reprogramming
and
promotes
drug
resistance.
We
aimed
to
explore
whether
a
novel
HSP90
inhibitor,
C210,
overcomes
doxorubicin
(DOX)
resistance
of
quiescent
breast
cancer
cells
by
targeting
TRAP1.
Breast
were
induced
quiescence
hypoxia
low
glucose.
The
relationship
cell
metabolism
with
was
investigated
Western
blotting,
ECAR,
OCR,
mitochondrial
complex
activity,
proteomic
analysis.
targets
C210
their
functions
analyzed
SPR
immunoprecipitation.
antitumor
effect
vivo
mouse
tumor
model.
In
glucose
deprivation,
exhibited
elevated
an
OXPHOS-enhanced
phenotype.
These
highly
resistant
DOX
but
more
sensitive
C210.
disrupted
TRAP1's
interaction
OXPHOS-associated
client
proteins,
prompting
proteasome-dependent
degradation
these
thereby
reducing
ATP
production
resulting
selective
elimination
the
inducing
apoptosis
which
could
be
reversed
exogenous
ATP.
Moreover,
targeted
glycolytic,
amino
acid,
β-oxidation-associated
proteome.
demonstrated
promising
anticancer
efficacy
particularly
related
OXPHOS
inhibition.
eliminates
DOX-resistant
TRAP1-dependent
bioenergetics.
Frontiers in Pharmacology,
Journal Year:
2023,
Volume and Issue:
14
Published: Oct. 17, 2023
Lactate
dehydrogenase
(LDH)
is
a
crucial
enzyme
involved
in
energy
metabolism
and
present
various
cells
throughout
the
body.
Its
diverse
physiological
functions
encompass
glycolysis,
its
abnormal
activity
associated
with
numerous
diseases.
Targeting
LDH
has
emerged
as
vital
approach
drug
discovery,
leading
to
identification
of
inhibitors
among
natural
compounds,
such
polyphenols,
alkaloids,
terpenoids.
These
compounds
demonstrate
therapeutic
potential
against
LDH-related
diseases,
including
anti-cancer
effects.
However,
challenges
concerning
limited
bioavailability,
poor
solubility,
toxicity
must
be
addressed.
Combining
led
promising
outcomes
preclinical
studies.
This
review
highlights
promise
for
treating
cancer,
cardiovascular,
neurodegenerative