Pharmaceutics,
Journal Year:
2020,
Volume and Issue:
12(11), P. 1084 - 1084
Published: Nov. 11, 2020
Doxorubicin
(DOX)
is
a
well-known
chemotherapeutic
agent
extensively
applied
in
the
field
of
cancer
therapy.
However,
similar
to
other
agents
such
as
cisplatin,
paclitaxel,
docetaxel,
etoposide
and
oxaliplatin,
cells
are
able
obtain
chemoresistance
that
limits
DOX
efficacy.
In
respect
dose-dependent
side
effect
DOX,
enhancing
its
dosage
not
recommended
for
effective
chemotherapy.
Therefore,
different
strategies
have
been
considered
reversing
resistance
diminishing
effects.
Phytochemical
potential
candidates
this
case
due
their
great
pharmacological
activities.
Curcumin
antitumor
phytochemical
isolated
from
Curcuma
longa
with
capacity
suppressing
metastasis
proliferation
affecting
molecular
pathways.
Experiments
demonstrated
curcumin
inhibiting
by
downregulating
oncogene
pathways
MMP-2,
TGF-β,
EMT,
PI3K/Akt,
NF-κB
AP-1.
Furthermore,
coadministration
potentiates
apoptosis
induction
cells.
light
this,
nanoplatforms
employed
codelivery
DOX.
This
results
promoting
bioavailability
internalization
aforementioned
active
compounds
and,
consequently,
activity.
Noteworthy,
has
reducing
adverse
effects
on
normal
tissues
via
inflammation,
oxidative
stress
apoptosis.
The
current
review
highlights
anticancer
mechanism,
nanovehicles.
Journal of Hematology & Oncology,
Journal Year:
2022,
Volume and Issue:
15(1)
Published: June 28, 2022
Abstract
Cancer
is
one
of
the
leading
causes
death
worldwide,
and
factors
responsible
for
its
progression
need
to
be
elucidated.
Exosomes
are
structures
with
an
average
size
100
nm
that
can
transport
proteins,
lipids,
nucleic
acids.
This
review
focuses
on
role
exosomes
in
cancer
therapy.
We
discuss
how
able
modulate
components
tumor
microenvironment
influence
proliferation
migration
rates
cells.
also
highlight
that,
depending
their
cargo,
suppress
or
promote
cell
enhance
reduce
response
radio-
chemo-therapies.
In
addition,
we
describe
trigger
chronic
inflammation
lead
immune
evasion
by
focusing
ability
transfer
non-coding
RNAs
between
cells
other
molecular
signaling
pathways
such
as
PTEN
PI3K/Akt
cancer.
Subsequently,
use
carriers
anti-tumor
agents
genetic
tools
control
progression.
then
tumor-derived
carcinogenesis.
Finally,
devote
a
section
study
diagnostic
prognostic
clinical
courses
important
treatment
patients.
provides
comprehensive
understanding
therapy,
therapeutic
value
remodeling
microenvironment.
Graphical
International Journal of Molecular Sciences,
Journal Year:
2020,
Volume and Issue:
21(11), P. 4002 - 4002
Published: June 3, 2020
Therapy
resistance
is
a
characteristic
of
cancer
cells
that
significantly
reduces
the
effectiveness
drugs.
Despite
popularity
cisplatin
(CP)
as
chemotherapeutic
agent,
which
widely
used
in
treatment
various
types
cancer,
to
CP
chemotherapy
has
been
extensively
observed.
Among
reported
mechanism(s),
epithelial-mesenchymal
transition
(EMT)
process
can
contribute
chemoresistance
by
converting
motionless
epithelial
into
mobile
mesenchymal
and
altering
cell-cell
adhesion
well
cellular
extracellular
matrix,
leading
invasion
tumor
cells.
By
analyzing
impact
different
molecular
pathways
such
microRNAs,
long
non-coding
RNAs,
nuclear
factor-κB
(NF-ĸB),
phosphoinositide
3-kinase-related
protein
kinase
(PI3K)/Akt,
mammalian
target
rapamycin
(mTOR),
Wnt,
play
an
important
role
exhibited
therapy,
we
first
give
introduction
about
EMT
mechanism
its
drug
resistance.
We
then
focus
specifically
on
involved
pharmacological
strategies
be
mitigate
this
Overall,
highlight
targeted
signaling
could
considered
future
studies
pave
way
for
inhibition
EMT-mediated
displayed
response
exposure.
Frontiers in Cell and Developmental Biology,
Journal Year:
2021,
Volume and Issue:
9
Published: June 10, 2021
Long
non-coding
RNAs
(lncRNAs)
regulate
gene
expression
in
a
variety
of
ways
at
epigenetic,
chromatin
remodeling,
transcriptional,
and
translational
levels.
Accumulating
evidence
suggests
that
lncRNA
X-inactive
specific
transcript
(lncRNA
Xist)
serves
as
an
important
regulator
cell
growth
development.
Despites
its
original
roles
X-chromosome
dosage
compensation,
Xist
also
participates
the
development
tumor
other
human
diseases
by
functioning
competing
endogenous
RNA
(ceRNA).
In
this
review,
we
comprehensively
summarized
recent
progress
understanding
cellular
functions
mammalian
cells
discussed
current
knowledge
regarding
ceRNA
network
various
diseases.
are
transcripts
more
than
200
nt
length
without
apparent
protein-coding
capacity
(Furlan
Rougeulle,
2016;
Maduro
et
al.,
2016).
These
believed
to
be
transcribed
approximately
98-99%
regions
genome
(Derrien
2012;
Fu,
2014;
Montalbano
2017;
Slack
Chinnaiyan,
2019),
well
large
genomic
regions,
such
exonic,
tronic,
intergenic
regions.
Hence,
lncRNAs
divided
into
eight
categories:
Intergenic
lncRNAs,
Intronic
Enhancer
Promoter
Natural
antisense/sense
Small
nucleolar
RNA-ended
(sno-lncRNAs),
Bidirectional
non-poly(A)
(Ma
2013;
Devaux
2015;
St
Laurent
Chen,
Quinn
Chang,
Richard
Eichhorn,
2018;
Connerty
2020).
A
range
has
suggested
function
key
regulators
crucial
functions,
including
proliferation,
differentiation,
apoptosis,
migration,
invasion,
regulating
level
target
genes
via
epigenomic,
or
post-transcriptional
approaches
(Cao
2018).
Moreover,
detected
body
fluids
were
serve
potential
biomarkers
for
diagnosis,
prognosis,
monitoring
disease
progression,
act
novel
drug
targets
therapeutic
exploitation
(Jiang
W.
Zhou
2019a).
set
15,000-20,000
sequences
localized
X
chromosome
inactivation
center
(XIC)
Xq13.2
(Brown
1992;
Debrand
1998;
Kay,
Lee
da
Rocha
Heard,
Yang
Z.
Brockdorff,
2019).
Previous
studies
have
indicated
(XCI),
resulting
inheritable
silencing
one
X-chromosomes
during
female
Also,
it
vital
regulatory
whole
spectrum
(notably
cancer)
can
used
diagnostic
prognostic
biomarker
clinic
(Liu
2018b;
Deng
2019;
Dinescu
Mutzel
Schulz,
2020;
Patrat
Wang
2020a).
particular,
been
demonstrated
involved
multiple
types
tumors
brain
tumor,
Leukemia,
lung
cancer,
breast
liver
with
prominent
examples
outlined
Table
1.
It
was
(Chaligne
2018)
contributed
diseases,
pulmonary
fibrosis,
inflammation,
neuropathic
pain,
cardiomyocyte
hypertrophy,
osteoarthritis
chondrocytes,
details
found
2.
This
review
summarizes
on
mechanisms
both
compensation
pathogenesis
(especially
processes,
focus
disease.
International Journal of Molecular Sciences,
Journal Year:
2020,
Volume and Issue:
21(9), P. 3285 - 3285
Published: May 6, 2020
Oral
cancer
(OC)
is
a
devastating
disease
that
takes
the
lives
of
lots
people
globally
every
year.
The
current
spectrum
treatment
modalities
does
not
meet
needs
patients.
heterogeneity
demands
personalized
medicine
or
targeted
therapies.
Therefore,
there
an
urgent
need
to
identify
potential
targets
for
OC.
Abundant
evidence
has
suggested
components
protein
kinase
B
(AKT)/
mammalian
target
rapamycin
(mTOR)
pathway
are
intrinsic
factors
carcinogenesis.
AKT
central
proliferation
and
survival
normal
cells,
its
downstream
protein,
mTOR,
also
plays
indispensable
role
in
cellular
processes.
wide
involvement
AKT/mTOR
been
noted
oral
squamous
cell
carcinoma
(OSCC).
This
axis
significantly
regulates
various
hallmarks
cancer,
like
proliferation,
survival,
angiogenesis,
invasion,
metastasis,
autophagy,
epithelial-to-mesenchymal
transition
(EMT).
Activated
signaling
associated
with
circadian
signaling,
chemoresistance
radio-resistance
OC
cells.
Several
miRNAs,
circRNAs
lncRNAs
modulate
this
pathway.
association
process
tumorigenesis
culminated
identification
specific
inhibitors
prevention
In
review,
we
discussed
significance
as
therapeutic
management
article
provided
update
on
several
emerged
promising
candidates
interventions
against
OC/head
neck
(HNC)
clinical
studies.
Biomedicine & Pharmacotherapy,
Journal Year:
2021,
Volume and Issue:
141, P. 111824 - 111824
Published: June 25, 2021
Epithelial-to-mesenchymal
transition
(EMT)
mechanism
is
responsible
for
metastasis
and
migration
of
cancer
cells
to
neighboring
tissues.
Morphologically,
epithelial
are
transformed
mesenchymal
cells,
at
molecular
level,
E-cadherin
undergoes
down-regulation,
while
an
increase
occurs
in
N-cadherin
vimentin
levels.
Increasing
evidence
demonstrates
role
EMT
mediating
drug
resistance
cells.
On
the
other
hand,
paclitaxel
(PTX)
docetaxel
(DTX)
two
chemotherapeutic
agents
belonging
taxene
family,
capable
inducing
cell
cycle
arrest
via
preventing
microtubule
depolymerization.
Aggressive
behavior
resulted
from
EMT-mediated
can
lead
PTX
DTX
resistance.
Upstream
mediators
such
as
ZEB1/2,
TGF-β,
microRNAs,
so
on
involved
regulating
response
DTX.
Tumor-suppressing
factors
inhibit
promote
sensitivity
Furthermore,
three
different
strategies
including
using
anti-tumor
compounds,
gene
therapy
delivery
systems
have
been
developed
suppressing
EMT,
enhancing
cytotoxicity
against
that
mechanistically
discussed
current
review.
Journal of Cellular Physiology,
Journal Year:
2022,
Volume and Issue:
237(7), P. 2770 - 2795
Published: May 13, 2022
Metastasis
of
tumor
cells
is
a
complex
challenge
and
significantly
diminishes
the
overall
survival
prognosis
cancer
patients.
The
epithelial-to-mesenchymal
transition
(EMT)
well-known
mechanism
responsible
for
invasiveness
cells.
A
number
molecular
pathways
can
regulate
EMT
in
nuclear
factor-kappaB
(NF-κB)
one
them.
translocation
NF-κB
p65
induce
transcription
several
genes
involved
induction.
present
review
describes
interaction
their
association
progression.
Due
to
oncogenic
role
signaling,
its
activation
enhances
metastasis
via
This
has
been
confirmed
various
cancers
including
brain,
breast,
lung
gastric
cancers,
among
others.
ZEB1/2,
transforming
growth
factor-β,
Slug
as
inducers
undergo
upregulation
by
promote
After
induction
driven
NF-κB,
significant
decrease
occurs
E-cadherin
levels,
while
N-cadherin
vimentin
levels
an
increase.
noncoding
RNAs
potentially
also
function
upstream
mediators
modulate
NF-κB/EMT
axis
cancers.
Moreover,
mediating
drug
resistance
Thus,
suppressing
sensitivity
chemotherapeutic
agents.
