Cancer
is
a
prominent
contributor
to
mortality
rates
globally,
with
its
progression
and
spread
being
the
primary
factors
underlying
this
assertion.
Despite
advancements
in
cancer
therapy,
existing
therapeutic
strategies
are
rendered
useless
as
result
of
their
toxicity
development
chemoresistance.
Hence,
it
imperative
assess
alternate
therapy
modalities,
natural
compounds
present
promising
prospect
due
demonstrated
anticancer
capabilities
several
research
models.
This
article
provides
an
overview
regulatory
mechanisms
involved
expression
metalloproteinases
(MMPs)
explores
potential
function
flavonoids
agents
activity
that
specifically
target
MMPs.
Multiple
indicate
chemopreventive
cytotoxic
against
wide
range
types,
according
data
gathered
from
cell
lines
vivo
Involved
invasion,
migration,
metastasis,
also
modulate
critical
signaling
pathways
including
signal
transducer
activator
transcription
3
(STAT3),
mitogen-activated
protein
kinase
(MAPK),
NFkB,
PI3/AKT.
All
these
findings
reestablish
outstanding
candidates
for
treatment.
Cellular and Molecular Life Sciences,
Год журнала:
2024,
Номер
81(1)
Опубликована: Фев. 9, 2024
Abstract
Metastasis
accounts
for
90%
of
cancer-related
deaths
among
the
patients.
The
transformation
epithelial
cells
into
mesenchymal
with
molecular
alterations
can
occur
during
epithelial–mesenchymal
transition
(EMT).
EMT
mechanism
accelerates
cancer
metastasis
and
drug
resistance
ability
in
human
cancers.
Among
different
regulators
EMT,
Wnt/β-catenin
axis
has
been
emerged
as
a
versatile
modulator.
Wnt
is
active
form
physiological
condition
due
to
function
GSK-3β
that
destructs
β-catenin,
while
ligand–receptor
interaction
impairs
increase
β-catenin
stability
promote
its
nuclear
transfer.
Regarding
oncogenic
Wnt/β-catenin,
upregulation
occurs
cancers
it
accelerate
EMT-mediated
resistance.
stimulation
by
binding
ligands
Frizzled
receptors
enhance
accumulation
cytoplasm
stimulates
related
genes
upon
translocation.
Wnt/β-catenin/EMT
implicated
augmenting
both
solid
hematological
tumors.
Wnt/EMT-mediated
promotes
malignant
behavior
tumor
cells,
causing
therapy
be
modulated
upstream
mediators
which
non-coding
RNAs
are
main
regulators.
Moreover,
pharmacological
intervention,
mainly
using
phytochemicals,
suppresses
Wnt/EMT
suppression.
Graphical
abstract
Cell Communication and Signaling,
Год журнала:
2024,
Номер
22(1)
Опубликована: Фев. 12, 2024
Abstract
Cancer
treatment
faces
many
hurdles
and
resistance
is
one
among
them.
Anti-cancer
strategies
are
evolving
due
to
innate
acquired
capacity,
governed
by
genetic,
epigenetic,
proteomic,
metabolic,
or
microenvironmental
cues
that
ultimately
enable
selected
cancer
cells
survive
progress
under
unfavorable
conditions.
Although
the
mechanism
of
drug
being
widely
studied
generate
new
target-based
drugs
with
better
potency
than
existing
ones.
However,
broader
flexibility
in
resistance,
advanced
therapeutic
options
efficacy
need
be
explored.
Combination
therapy
an
alternative
a
success
rate
though
risk
amplified
side
effects
commonplace.
Moreover,
recent
groundbreaking
precision
immune
ways
overcome
has
revolutionized
anticancer
greater
extent
only
limitation
individual-specific
needs
further
attention.
This
review
will
focus
on
challenges
opted
withstand
current
therapies
at
molecular
level
also
highlights
emerging
-like
immunological,
stem
cell-based
may
prove
have
potential
challenge
problem
resistance.
Cellular and Molecular Life Sciences,
Год журнала:
2024,
Номер
81(1)
Опубликована: Май 11, 2024
The
non-coding
RNAs
comprise
a
large
part
of
human
genome
lack
capacity
in
encoding
functional
proteins.
Among
various
members
RNAs,
the
circular
(circRNAs)
have
been
importance
pathogenesis
diseases,
especially
cancer.
circRNAs
unique
closed
loop
structure
and
due
to
their
stability,
they
are
potential
diagnostic
prognostic
factors
increasing
evidences
highlighted
role
modulation
proliferation
metastasis
cancer
cells.
On
other
hand,
has
responsible
for
up
90%
cancer-related
deaths
patients,
requiring
more
investigation
regarding
underlying
mechanisms
modulating
this
mechanism.
EMT
enhances
invasion
tumor
cells,
can
trigger
resistance
therapy.
cells
demonstrate
dynamic
changes
during
including
transformation
from
epithelial
phenotype
into
mesenchymal
increase
N-cadherin
vimentin
levels.
process
is
reversible
its
reprogramming
disrupt
progression
aim
current
review
understanding
interaction
cancers
such
beyond
regulation
affect
response
chemotherapy
radiotherapy.
onco-suppressor
inhibit
EMT,
while
tumor-promoting
mediate
acceleration
carcinogenesis.
Moreover,
EMT-inducing
transcription
be
controlled
by
different
tumors.
Cancers,
Год журнала:
2024,
Номер
16(17), С. 2975 - 2975
Опубликована: Авг. 27, 2024
Malignant
gliomas
present
great
difficulties
in
treatment,
with
little
change
over
the
past
30
years
median
survival
time
of
15
months.
Current
treatment
options
include
surgery,
radiotherapy
(RT),
and
chemotherapy.
New
therapies
aimed
at
suppressing
formation
new
vasculature
(antiangiogenic
treatments)
or
destroying
formed
tumor
(vascular
disrupting
agents)
show
promise.
This
study
summarizes
existing
knowledge
regarding
processes
by
which
glioblastoma
(GBM)
tumors
acquire
resistance
to
antiangiogenic
treatments.
The
discussion
encompasses
activation
redundant
proangiogenic
pathways,
heightened
cell
invasion
metastasis,
induced
hypoxia,
creation
vascular
mimicry
channels,
regulation
immune
microenvironment.
Subsequently,
we
explore
potential
strategies
overcome
this
resistance,
such
as
combining
other
methods,
personalizing
treatments
for
each
patient,
focusing
on
therapeutic
targets,
incorporating
immunotherapy,
utilizing
drug
delivery
systems
based
nanoparticles.
Additionally,
would
like
discuss
limitations
methods
future
directions
enhance
beneficial
effects
patients
GBM.
Therefore,
review
aims
research
outcome
GBM
provide
a
more
promising
opportunity
thoroughly
exploring
mechanisms
investigating
novel
strategies.
