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 Experimental & Clinical Cancer Research,
Journal Year:
2022,
Volume and Issue:
41(1)
Published: July 1, 2022
Abstract
Background
One
of
the
most
malignant
tumors
in
men
is
prostate
cancer
that
still
incurable
due
to
its
heterogenous
and
progressive
natures.
Genetic
epigenetic
changes
play
significant
roles
development.
The
RNA
molecules
with
more
than
200
nucleotides
length
are
known
as
lncRNAs
these
factors
do
not
encode
protein.
They
regulate
gene
expression
at
transcriptional,
post-transcriptional
levels.
LncRNAs
vital
biological
functions
cells
pathological
events,
hence
their
undergoes
dysregulation.
Aim
review
role
alterations
development
emphasized
here.
Therefore,
were
chosen
for
this
purpose
level
interaction
other
signaling
networks
progression
examined.
Key
scientific
concepts
aberrant
has
been
well-documented
rate
tumor
regulated
via
affecting
STAT3,
NF-κB,
Wnt,
PI3K/Akt
PTEN,
among
molecular
pathways.
Furthermore,
radio-resistance
chemo-resistance
features
cells.
Overexpression
tumor-promoting
such
HOXD-AS1
CCAT1
can
result
drug
resistance.
Besides,
induce
immune
evasion
upregulating
PD-1.
Pharmacological
compounds
quercetin
curcumin
have
applied
targeting
lncRNAs.
siRNA
tool
reduce
thereby
suppressing
progression.
Prognosis
diagnosis
clinical
course
be
evaluated
by
exosomal
lncRNA-p21
investigated
serum
patients
a
reliable
biomarker.
Cancers,
Journal Year:
2021,
Volume and Issue:
13(8), P. 1882 - 1882
Published: April 14, 2021
In
cancer
cells,
a
vital
cellular
process
during
metastasis
is
the
transformation
of
epithelial
cells
towards
motile
mesenchymal
called
to
transition
(EMT).
The
cytoskeleton
an
active
network
three
intracellular
filaments:
actin
cytoskeleton,
microtubules,
and
intermediate
filaments.
These
filaments
play
central
role
in
structural
design
cell
behavior
are
necessary
for
EMT.
During
EMT,
undergo
as
manifested
by
elongation,
migration,
invasion,
coordinated
reorganization.
extremely
dynamic
structure,
controlled
balance
assembly
disassembly
Actin-binding
proteins
regulate
polymerization
depolymerization.
Microtubule
reorganization
also
plays
important
migration
polarization.
Intermediate
rearranged,
switching
vimentin-rich
network,
this
protein
used
marker
cell.
Hence,
targeting
EMT
regulating
activities
their
key
components
may
be
potential
solution
metastasis.
This
review
summarizes
research
done
on
physiological
functions
its
process,
effect
multidrug-resistant
(MDR)
cells—highlight
some
future
perspectives
therapy
cytoskeleton.
Medicinal Research Reviews,
Journal Year:
2023,
Volume and Issue:
43(4), P. 1141 - 1200
Published: March 17, 2023
Abstract
Epithelial‐mesenchymal
transition
(EMT)
is
a
complex
process
with
primordial
role
in
cellular
transformation
whereby
an
epithelial
cell
transforms
and
acquires
mesenchymal
phenotype.
This
plays
pivotal
tumor
progression
self‐renewal,
exacerbates
resistance
to
apoptosis
chemotherapy.
EMT
can
be
initiated
promoted
by
deregulated
oncogenic
signaling
pathways,
hypoxia,
cells
the
microenvironment,
resulting
loss‐of‐epithelial
polarity,
cell–cell
adhesion,
enhanced
invasive/migratory
properties.
Numerous
transcriptional
regulators,
such
as
Snail,
Slug,
Twist,
ZEB1/ZEB2
induce
through
downregulation
of
markers
gain‐of‐expression
markers.
Additionally,
cascades
Wnt/β‐catenin,
Notch,
Sonic
hedgehog,
nuclear
factor
kappa
B,
receptor
tyrosine
kinases,
PI3K/AKT/mTOR,
Hippo,
transforming
growth
factor‐β
pathways
regulate
whereas
they
are
often
cancers
leading
aberrant
EMT.
Furthermore,
noncoding
RNAs,
tumor‐derived
exosomes,
epigenetic
alterations
also
involved
modulation
Therefore,
regulation
vital
strategy
control
aggressive
metastatic
characteristics
cells.
Despite
vast
amount
preclinical
data
on
cancer
progression,
there
lack
clinical
translation
at
therapeutic
level.
In
this
review,
we
have
discussed
thoroughly
aforementioned
transcription
factors,
RNAs
(microRNAs,
long
RNA,
circular
RNA),
modifications,
exosomes
cancers.
We
emphasized
contribution
drug
possible
interventions
using
plant‐derived
natural
products,
their
semi‐synthetic
derivatives,
nano‐formulations
that
described
promising
blockers.
Journal of Experimental & Clinical Cancer Research,
Journal Year:
2022,
Volume and Issue:
41(1)
Published: March 22, 2022
Abstract
Prostate
cancer
is
a
leading
cause
of
death
worldwide
and
new
estimates
revealed
prostate
as
the
in
men
2021.
Therefore,
strategies
are
pertinent
treatment
this
malignant
disease.
Macroautophagy/autophagy
“self-degradation”
mechanism
capable
facilitating
turnover
long-lived
toxic
macromolecules
organelles.
Recently,
attention
has
been
drawn
towards
role
autophagy
how
its
modulation
provides
effective
therapy.
In
present
review,
we
provide
mechanistic
discussion
cancer.
Autophagy
can
promote/inhibit
proliferation
survival
cells.
Besides,
metastasis
cells
affected
(via
induction
inhibition)
by
autophagy.
affect
response
to
therapy
such
chemotherapy
radiotherapy,
given
close
association
between
apoptosis.
Increasing
evidence
demonstrated
that
upstream
mediators
AMPK,
non-coding
RNAs,
KLF5,
MTOR
others
regulate
Anti-tumor
compounds,
for
instance
phytochemicals,
dually
inhibit
or
induce
For
improving
therapy,
nanotherapeutics
chitosan
nanoparticles
have
developed.
With
respect
context-dependent
cancer,
genetic
tools
siRNA
CRISPR-Cas9
be
utilized
targeting
autophagic
genes.
Finally,
these
findings
translated
into
preclinical
clinical
studies
improve
prognosis
patients.
Graphical
abstract
Pharmacological Research,
Journal Year:
2022,
Volume and Issue:
187, P. 106553 - 106553
Published: Nov. 16, 2022
Cancer
progression
results
from
activation
of
various
signaling
networks.
Among
these,
PI3K/Akt
contributes
to
proliferation,
invasion,
and
inhibition
apoptosis.
Hepatocellular
carcinoma
(HCC)
is
a
primary
liver
cancer
with
high
incidence
rate,
especially
in
regions
prevalence
viral
hepatitis
infection.
Autoimmune
disorders,
diabetes
mellitus,
obesity,
alcohol
consumption,
inflammation
can
also
lead
initiation
development
HCC.
The
treatment
HCC
depends
on
the
identification
oncogenic
factors
that
tumor
cells
develop
resistance
therapy.
present
review
article
focuses
role
progression.
Activation
promotes
glucose
uptake,
favors
glycolysis
increases
cell
proliferation.
It
inhibits
both
apoptosis
autophagy
while
promoting
survival.
stimulates
epithelial-to-mesenchymal
transition
(EMT)
matrix-metalloproteinase
(MMP)
expression
during
metastasis.
In
addition
increasing
colony
formation
capacity
facilitating
spread
cells,
angiogenesis.
Therefore,
silencing
prevents
aggressive
behavior.
confer
drug
resistance,
particularly
sorafenib,
decreases
radio-sensitivity
cells.
Anti-cancer
agents,
like
phytochemicals
small
molecules
suppress
by
limiting
Being
upregulated
tissues
clinical
samples,
be
used
as
biomarker
predict
patients'
response
Medicinal Research Reviews,
Journal Year:
2023,
Volume and Issue:
43(5), P. 1263 - 1321
Published: March 23, 2023
Abstract
Gastrointestinal
(GI)
tumors
(cancers
of
the
esophagus,
gastric,
liver,
pancreas,
colon,
and
rectum)
contribute
to
a
large
number
deaths
worldwide.
STAT3
is
an
oncogenic
transcription
factor
that
promotes
genes
associated
with
proliferation,
antiapoptosis,
survival,
metastasis.
overactivated
in
many
human
malignancies
including
GI
which
accelerates
tumor
progression,
metastasis,
drug
resistance.
Research
recent
years
demonstrated
noncoding
RNAs
(ncRNAs)
play
major
role
regulation
signaling
pathways
pathway.
The
types
endogenous
ncRNAs
are
being
extensively
studied
oncology
microRNAs,
long
RNAs,
circular
RNAs.
These
can
either
be
tumor‐promoters
or
tumor‐suppressors
each
one
them
imparts
their
activity
via
different
mechanisms.
pathway
also
tightly
modulated
by
ncRNAs.
In
this
article,
we
have
elaborated
on
tumor‐promoting
tumors.
Subsequently,
comprehensively
discussed
as
well
suppressor
functions
mechanism
action
known
modulate
cancers.
Cancers,
Journal Year:
2024,
Volume and Issue:
16(2), P. 259 - 259
Published: Jan. 6, 2024
Metabolic-dysfunction-associated
steatotic
liver
disease
(MASLD,
previously
known
as
non-alcoholic
fatty
(NAFLD))
represents
a
rapidly
increasing
cause
of
chronic
and
hepatocellular
carcinoma
(HCC),
mirroring
rates
obesity
metabolic
syndrome
in
the
Western
world.
MASLD-HCC
can
develop
at
an
earlier
stage
fibrosis
compared
to
other
causes
disease,
presenting
challenges
how
risk-stratify
patients
set
up
effective
screening
programmes.
Therapeutic
decision
making
for
is
also
complicated
by
medical
comorbidities
presentation
later
stage.
The
response
treatment,
particularly
immune
checkpoint
inhibitors,
may
vary
aetiology
and,
future,
patient
stratification
will
be
key
optimizing
therapeutic
pathways.