Cell Death and Disease,
Journal Year:
2023,
Volume and Issue:
14(8)
Published: Aug. 17, 2023
Abstract
Despite
the
advancements
made
in
diagnosis
and
treatment
of
cancer,
stages
associated
with
metastasis
remain
largely
incurable
represent
primary
cause
cancer-related
deaths.
The
dissemination
cancer
is
facilitated
by
circulating
tumor
cells
(CTCs),
which
originate
from
or
metastatic
sites
enter
bloodstream,
subsequently
spreading
to
distant
parts
body.
CTCs
have
garnered
significant
attention
research
due
their
accessibility
peripheral
blood,
despite
low
abundance.
They
are
being
extensively
studied
gain
a
deeper
understanding
mechanisms
underlying
identify
effective
therapeutic
strategies
for
advanced
disease.
Therefore,
substantial
efforts
been
directed
towards
establishing
characterizing
relevant
experimental
models
derived
CTCs,
aiming
provide
tools
research.
In
this
review,
we
an
overview
recent
progress
establishment
preclinical
CTC-derived
models,
such
as
xenografts
(CDX)
cell
cultures,
show
promise
study
CTCs.
We
discuss
advantages
limitations
these
conclude
summarizing
potential
future
use
decisions
utility
precision
medicine
tools.
Cancers,
Journal Year:
2020,
Volume and Issue:
12(2), P. 287 - 287
Published: Jan. 24, 2020
Chemokines
are
chemotactic
cytokines
that
mediate
immune
cell
chemotaxis
and
lymphoid
tissue
development.
Recent
advances
have
indicated
chemokines
their
cognate
receptors
play
critical
roles
in
cancer-related
inflammation
cancer
progression.
On
the
basis
of
these
findings,
chemokine
system
has
become
a
new
potential
drug
target
for
immunotherapy.
In
this
review,
we
summarize
essential
complex
network
Furthermore,
discuss
value
as
prognostic
marker.
The
regulates
infiltration
cells
into
tumor
microenvironment,
which
induces
both
pro-
anti-immunity
promotes
or
suppresses
growth
proliferation,
angiogenesis,
metastasis.
Increasing
evidence
indicates
promising
patients.
While
CCL2,
CXCL10,
CX3CL1/CX3CR1
can
serve
favorable
unfavorable
factors
depending
on
types,
CCL14
XCL1
possess
good
value.
Other
such
CXCL1,
CXCL8,
CXCL12
poor
markers.
Despite
vast
our
understanding
nature
biology,
knowledge
about
multifaceted
different
types
cancers
is
still
limited.
Further
studies
necessary
to
decipher
distinct
within
terms
progression
validate
prognosis.
Frontiers in Molecular Biosciences,
Journal Year:
2020,
Volume and Issue:
7
Published: April 30, 2020
Intratumoral
heterogeneity
is
a
major
ongoing
challenge
in
the
effective
therapeutic
targeting
of
cancer.
Accumulating
evidence
suggests
that
fraction
cells
within
tumor
termed
Cancer
Stem
Cells
(CSCs)
are
primarily
responsible
for
this
diversity
resulting
resistance
and
metastasis.
Adding
to
complexity,
recent
studies
have
shown
there
can
be
different
subpopulations
CSCs
with
varying
biochemical
biophysical
traits
varied
dissemination
drug-resistance
potential.
Moreover,
cancer
exhibit
high
level
plasticity
or
ability
dynamically
switch
between
CSC
non-CSC
statesoramong
subsets
CSCs.
The
molecular
mechanisms
underlying
such
has
been
under
extensive
investigation
trans-differentiation
process
Epithelial
Mesenchymal
transition
(EMT)
identified
as
contributing
factor.
Besides
genetic
epigenetic
factors,
also
shaped
by
non-cell-autonomous
effects
microenvironment.
In
review,
we
discuss
developments
understanding
progression
at
levels,and
latest
silico
approaches
being
taken
characterizing
cell
implications
improving
existing
approaches.
Frontiers in Immunology,
Journal Year:
2023,
Volume and Issue:
14
Published: Nov. 16, 2023
Cancer
progression
is
primarily
caused
by
interactions
between
transformed
cells
and
the
components
of
tumor
microenvironment
(TME).
TAMs
(tumor-associated
macrophages)
make
up
majority
invading
immune
components,
which
are
further
categorized
as
anti-tumor
M1
pro-tumor
M2
subtypes.
While
known
to
have
anti-cancer
properties,
recognized
extend
a
protective
role
tumor.
As
result,
manipulates
TME
in
such
way
that
it
induces
macrophage
infiltration
switching
bias
secure
its
survival.
This
M2-TAM
promotes
cancer
cell
proliferation,
neoangiogenesis,
lymphangiogenesis,
epithelial-to-mesenchymal
transition,
matrix
remodeling
for
metastatic
support,
manipulation
an
immunosuppressive
state.
additionally
promote
emergence
stem
(CSCs),
their
ability
originate,
metastasize,
relapse
into
tumors.
CSCs
also
help
revealing
escape
survival
strategies
during
initiation
phases.
review
describes
reasons
immunotherapy
failure
and,
thereby,
devises
better
impair
tumor-TAM
crosstalk.
study
will
shed
light
on
understudied
TAM-mediated
address
much-needed
holistic
approach
therapy,
encompasses
targeting
cells,
CSCs,
all
at
same
time.
Cell Communication and Signaling,
Journal Year:
2022,
Volume and Issue:
20(1)
Published: June 17, 2022
Triple-negative
breast
cancer
(TNBC)
is
a
highly
aggressive
subtype
of
with
poor
prognosis
and
limited
treatment.
As
major
component
the
tumor
microenvironment,
tumor-associated
macrophages
(TAMs)
play
an
important
role
in
facilitating
behavior
TNBC.
This
study
aimed
to
explore
novel
mechanism
TAMs
regulation
epithelial-mesenchymal
transition
(EMT)
stem
cell
(CSC)
properties
TNBC.Expression
M2-like
macrophage
marker
CD163
was
evaluated
by
immunohistochemistry
human
tissues.
The
phenotype
M2
polarized
from
Tohoku-Hospital-Pediatrics-1
(THP1)
cells
verified
flow
cytometry.
Transwell
assays,
wound
healing
western
blotting,
cytometry,
ELISA,
quantitative
polymerase
chain
reaction
(qPCR),
luciferase
reporter
gene
immunofluorescence
assays
were
conducted
investigate
which
regulate
EMT
CSC
BT549
HCC1937
cells.Clinically,
we
observed
high
infiltration
TNBC
tissues
confirmed
that
associated
unfavorable
patients.
Moreover,
found
conditioned
medium
(M2-CM)
markedly
promoted
cells.
Mechanistically,
demonstrated
chemokine
(C-C
motif)
ligand
2
(CCL2)
secretion
activated
Akt
signaling,
turn
increased
expression
nuclear
localization
β-catenin.
Furthermore,
β-catenin
knockdown
reversed
TAM-induced
properties.This
provides
promote
enhance
via
activation
CCL2/AKT/β-catenin
may
offer
new
strategies
for
diagnosis
treatment
Video
Abstract.
Cancer and Metastasis Reviews,
Journal Year:
2024,
Volume and Issue:
43(1), P. 197 - 228
Published: Feb. 8, 2024
Abstract
Cancer
is
a
complex
disease
displaying
variety
of
cell
states
and
phenotypes.
This
diversity,
known
as
cancer
plasticity,
confers
cells
the
ability
to
change
in
response
their
environment,
leading
increased
tumor
diversity
drug
resistance.
review
explores
intricate
landscape
offering
deep
dive
into
cellular,
molecular,
genetic
mechanisms
that
underlie
this
phenomenon.
plasticity
intertwined
with
processes
such
epithelial-mesenchymal
transition
acquisition
stem
cell–like
features.
These
are
pivotal
development
progression
tumors,
contributing
multifaceted
nature
challenges
associated
its
treatment.
Despite
significant
advancements
targeted
therapies,
adaptability
subsequent
therapy-induced
resistance
remain
persistent
obstacles
achieving
consistent,
successful
treatment
outcomes.
Our
delves
array
exploit
maintain
including
epigenetic
modifications,
alterations
signaling
pathways,
environmental
interactions.
We
discuss
strategies
counteract
targeting
specific
cellular
pathways
employing
combination
therapies.
promise
enhance
efficacy
treatments
mitigate
therapy
In
conclusion,
offers
holistic,
detailed
exploration
aiming
bolster
understanding
approach
toward
tackling
posed
by
heterogeneity
As
articulated
review,
delineation
underlying
seeks
contribute
substantially
progress
therapeutics
advancement
precision
medicine,
ultimately
enhancing
prospects
for
effective
patient
Frontiers in Oncology,
Journal Year:
2020,
Volume and Issue:
10
Published: June 2, 2020
Multidrug
resistance
(MDR),
which
is
a
significant
impediment
to
the
success
of
cancer
chemotherapy,
attributable
various
defensive
mechanisms
in
cancer.
Initially,
overexpression
ATP-binding
cassette
(ABC)
transporters
such
as
P-glycoprotein
(P-gp)
was
considered
most
important
mechanism
for
drug
resistance;
hence,
many
investigators
long
time
focused
on
development
specific
ABC
transporter
inhibitors.
However,
date
their
efforts
have
failed
develop
clinically
applicable
drug,
leaving
only
number
problems.
The
concept
stem
cells
(CSCs)
has
provided
new
directions
both
and
MDR
research.
known
be
one
features
CSCs
thus
plays
crucial
role
recurrence
exacerbation.
Therefore,
recent
years,
research
targeting
been
increasing
rapidly
search
an
effective
treatment.
Here,
we
review
drugs
that
studied
developed
overcome
CSCs,
discuss
limitations
future
perspectives.
Journal of Clinical Investigation,
Journal Year:
2021,
Volume and Issue:
131(1)
Published: Jan. 3, 2021
Interferons
(IFNs)
are
pleiotropic
cytokines
critical
for
regulation
of
epithelial
cell
functions
and
immune
system
regulation.
In
cancer,
IFNs
contribute
to
tumor-intrinsic
-extrinsic
mechanisms
that
determine
the
quality
antitumor
immunity
response
immunotherapy.
this
Review,
we
focus
on
different
types
tumor
IFN
sensitivity
dynamic
tumor-immune
interactions
their
coevolution
during
cancer
progression
metastasis.
We
extend
discussion
new
evidence
supporting
immunotherapy-mediated
immunoediting
dual
opposing
roles
lead
checkpoint
blockade
or
resistance.
Understanding
intricate
responses
will
novel
immunotherapeutic
strategies
circumvent
protumorigenic
effects
while
exploiting
IFN-mediated
immunity.
Frontiers in Oncology,
Journal Year:
2021,
Volume and Issue:
11
Published: Aug. 12, 2021
The
E2F
family
of
transcription
factors
(E2Fs)
consist
eight
genes
in
mammals.
These
encode
ten
proteins
that
are
usually
classified
as
transcriptional
activators
or
repressors.
E2Fs
important
for
many
cellular
processes,
from
their
canonical
role
cell
cycle
regulation
to
other
roles
angiogenesis,
the
DNA
damage
response
and
apoptosis.
A
growing
body
evidence
demonstrates
cancer
stem
cells
(CSCs)
key
players
tumor
development,
metastasis,
drug
resistance
recurrence.
This
review
focuses
on
CSCs
notes
signals
can
regulate
activities
E2Fs,
which
turn
transcriptionally
different
targets
contribute
various
biological
characteristics
CSCs,
such
proliferation,
self-renewal,
resistance.
Therefore,
may
be
promising
biomarkers
therapeutic
associated
with
pathologies.
Finally,
exploring
strategies
result
disruption
prevent
growth,