Pharmaceutics,
Journal Year:
2022,
Volume and Issue:
14(4), P. 866 - 866
Published: April 15, 2022
A
key
issue
with
modern
cancer
treatments
is
the
emergence
of
resistance
to
conventional
chemotherapy
and
molecularly
targeted
medicines.
Cancer
nanotherapeutics
were
created
in
order
overcome
inherent
limitations
traditional
chemotherapeutics.
Over
last
few
decades,
provided
unparalleled
opportunities
understand
drug
through
clinical
assessment
rationally
designed
nanoparticulate
delivery
systems.
In
this
context,
various
design
strategies
such
as
passive
targeting,
active
nano-drug,
multimodal
nano-drug
combination
therapy
effective
treatment.
Even
though
nanotherapy
has
made
great
technological
progress,
tumor
biology
complexity
heterogeneity
a
lack
comprehensive
knowledge
nano-bio
interactions
remain
important
roadblocks
future
translation
commercialization.
The
current
developments
advancements
employing
wide
variety
nanomaterial-based
platforms
treatment
are
discussed
article.
There
also
review
nanotherapeutics-based
approaches
therapy,
including
targeting
for
microenvironment
its
components,
advanced
systems
specific
stem
cells
(CSC),
well
exosomes
strategies,
an
update
on
trials.
Finally,
challenges
perspective
reverse
discussed.
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(15), P. 12222 - 12222
Published: July 30, 2023
One
of
the
leading
causes
death
worldwide,
in
both
men
and
women,
is
cancer.
Despite
significant
development
therapeutic
strategies,
inevitable
emergence
drug
resistance
limits
success
impedes
curative
outcome.
Intrinsic
acquired
are
common
mechanisms
responsible
for
cancer
relapse.
Several
factors
crucially
regulate
tumourigenesis
resistance,
including
physical
barriers,
tumour
microenvironment
(TME),
heterogeneity,
genetic
epigenetic
alterations,
immune
system,
burden,
growth
kinetics
undruggable
targets.
Moreover,
transforming
factor-beta
(TGF-β),
Notch,
epidermal
factor
receptor
(EGFR),
integrin-extracellular
matrix
(ECM),
nuclear
kappa-light-chain-enhancer
activated
B
cells
(NF-κB),
phosphoinositol-3-kinase/protein
kinase
B/mammalian
target
rapamycin
(PI3K/Akt/mTOR),
wingless-related
integration
site
(Wnt/β-catenin),
Janus
kinase/signal
transducers
activators
transcription
(JAK/STAT)
RAS/RAF/mitogen-activated
protein
(MAPK)
signalling
pathways
some
key
players
that
have
a
pivotal
role
mechanisms.
To
guide
future
treatments
improve
results,
deeper
comprehension
necessary.
This
review
covers
intrinsic
gives
comprehensive
overview
recent
research
on
enable
to
bypass
barriers
put
up
by
treatments,
and,
like
“satellite
navigation”,
find
alternative
routes
which
carry
their
“journey”
progression.
Cancer Communications,
Journal Year:
2024,
Volume and Issue:
44(4), P. 469 - 490
Published: March 21, 2024
Abstract
Background
Chemoresistance
is
a
major
cause
of
treatment
failure
in
gastric
cancer
(GC).
Heterogeneous
nuclear
ribonucleoprotein
A2B1
(hnRNPA2B1)
an
N6‐methyladenosine
(m
6
A)‐binding
protein
involved
variety
cancers.
However,
whether
m
A
modification
and
hnRNPA2B1
play
role
GC
chemoresistance
largely
unknown.
In
this
study,
we
aimed
to
investigate
the
downstream
mechanism
chemoresistance.
Methods
The
expression
among
public
datasets
were
analyzed
validated
by
quantitative
PCR
(qPCR),
Western
blotting,
immunofluorescence,
immunohistochemical
staining.
biological
functions
investigated
both
vitro
vivo.
RNA
sequencing,
methylated
immunoprecipitation,
stability
assay
performed
assess
association
between
binding
RNA.
maintenance
stemness
was
evaluated
bioinformatic
analysis,
qPCR,
sphere
formation
assays.
patterns
regulators
specimens
from
patients
who
received
adjuvant
chemotherapy
RNAscope
multiplex
immunohistochemistry.
Results
Elevated
found
cells
tissues,
especially
multidrug‐resistant
(MDR)
cell
lines.
associated
with
poor
outcomes
patients,
those
5‐fluorouracil
treatment.
Silencing
effectively
sensitized
inhibiting
proliferation
inducing
apoptosis
Mechanically,
interacted
stabilized
long
noncoding
NEAT1
A‐dependent
manner.
Furthermore,
worked
together
enhance
properties
via
Wnt/β‐catenin
signaling
pathway.
clinical
subjected
chemotherapy,
levels
hnRNPA2B1,
NEAT1,
CD133,
CD44
markedly
elevated
non‐responders
compared
responders.
Conclusion
Our
findings
indicated
that
interacts
stabilizes
lncRNA
which
contribute
property
pathway
exacerbate
GC.
Cancers,
Journal Year:
2024,
Volume and Issue:
16(4), P. 680 - 680
Published: Feb. 6, 2024
In
recent
years,
the
emergence
of
cancer
drug
resistance
has
been
one
crucial
tumor
hallmarks
that
are
supported
by
level
genetic
heterogeneity
and
complexities
at
cellular
levels.
Oxidative
stress,
immune
evasion,
metabolic
reprogramming,
overexpression
ABC
transporters,
stemness
among
several
key
contributing
molecular
response
mechanisms.
Topo-active
drugs,
e.g.,
doxorubicin
topotecan,
clinically
active
utilized
extensively
against
a
wide
variety
human
tumors
often
result
in
development
failure
to
therapy.
Thus,
there
is
an
urgent
need
for
incremental
comprehensive
understanding
mechanisms
specifically
context
topo-active
drugs.
This
review
delves
into
intricate
mechanistic
aspects
these
intracellular
extracellular
explores
use
potential
combinatorial
approaches
utilizing
various
drugs
inhibitors
pathways
involved
resistance.
We
believe
this
will
help
guide
basic
scientists,
pre-clinicians,
clinicians,
policymakers
toward
holistic
interdisciplinary
strategies
transcend
resistance,
renewing
optimism
ongoing
battle
cancer.
Cancer Communications,
Journal Year:
2021,
Volume and Issue:
41(10), P. 981 - 1006
Published: July 20, 2021
Oral
squamous
cell
carcinoma
(OSCC),
the
eighth
most
prevalent
cancer
in
world,
arises
from
interaction
of
multiple
factors
including
tobacco,
alcohol
consumption,
and
betel
quid.
Chemotherapeutic
agents
such
as
cisplatin,
5-fluorouracil,
paclitaxel
have
now
become
first-line
options
for
OSCC
patients.
Nevertheless,
patients
eventually
acquire
drug
resistance,
leading
to
poor
prognosis.
With
discovery
identification
non-coding
RNAs
(ncRNAs),
functions
dysregulated
ncRNAs
development
resistance
are
gradually
being
widely
recognized.
The
mechanisms
intricate
involve
efflux,
epithelial-mesenchymal
transition,
DNA
damage
repair,
autophagy.
At
present,
strategies
explore
reversal
need
be
urgently
developed.
Nano-delivery
self-cellular
delivery
platforms
considered
effective
overcome
due
their
tumor
targeting,
controlled
release,
consistent
pharmacokinetic
profiles.
In
particular,
combined
application
new
technologies
(including
CRISPR
systems)
opened
up
horizons
treatment
OSCC.
Hence,
this
review
explored
emerging
regulatory
OSCC,
elucidated
ncRNA-meditated
discussed
potential
value
using
nanoparticles
self-cells
carriers
FEBS Journal,
Journal Year:
2021,
Volume and Issue:
289(24), P. 7970 - 7986
Published: Sept. 3, 2021
CD44,
a
non-kinase
transmembrane
glycoprotein,
is
ubiquitously
expressed
on
various
types
of
cells,
especially
cancer
stem
cells
(CSCs),
and
has
been
implicated
in
onset
aggressiveness.
The
major
ligand
for
the
hyaluronan
(HA),
binds
to
interacts
with
which
turn
triggers
downstream
signaling
cascades,
thereby
promoting
cellular
behaviors
such
as
proliferation,
motility,
invasiveness
chemoresistance.
CD44-HA
interaction
cell-specific
strongly
affected
by
state
CD44
activation.
Therefore,
binding
HA
essential
activation
during
detailed
regulatory
mechanism
needs
be
clarified.
Different
states
distribute
human
carcinoma
normal
tissue;
however,
whether
critical
requirement
tumor
initiation,
progression
notorious
CSC
properties
remains
A
deeper
understanding
regulation
may
facilitate
development
novel
targeted
drugs
future.
Here,
we
review
current
findings
concerning
cell
surface,
underlying
mechanisms
activation,
known
role
hallmarks,
well
potential
HA-coated
nanoparticle
targeting
activated
therapy.
Frontiers in Oncology,
Journal Year:
2021,
Volume and Issue:
11
Published: Oct. 22, 2021
Oral
squamous
cell
carcinoma
(OSCC)
is
a
kind
of
malignant
tumors
with
low
survival
rate
and
prone
to
have
early
metastasis
recurrence.
Cisplatin
an
alkylating
agent
which
induces
DNA
damage
through
the
formation
cisplatin-DNA
adducts,
leading
cycle
arrest
apoptosis.
In
management
advanced
OSCC,
cisplatin-based
chemotherapy
or
chemoradiotherapy
has
been
considered
as
first-line
treatment.
Unfortunately,
only
portion
OSCC
patients
can
benefit
from
cisplatin
treatment,
both
inherent
resistance
acquired
greatly
limit
efficacy
even
cause
treatment
failure.
Herein,
this
review
outline
underlying
mechanisms
in
aspects
repair,
epigenetic
regulation,
transport
processes,
programmed
death
tumor
microenvironment.
addition,
summarizes
strategies
applicable
overcome
resistance,
provide
new
ideas
improve
clinical
therapeutic
outcome
OSCC.