Frontiers in Immunology,
Journal Year:
2021,
Volume and Issue:
12
Published: Dec. 20, 2021
Immunotherapy
holds
great
promise
for
treating
cancer.
Nonetheless,
T
cell-based
immunotherapy
of
solid
tumors
has
remained
challenging,
largely
due
to
the
lack
universal
tumor-specific
antigens
and
an
immunosuppressive
tumor
microenvironment
(TME)
that
inhibits
lymphocyte
infiltration
activation.
Aberrant
vascularity
characterizes
malignant
tumors,
which
fuels
formation
immune-hostile
induces
resistance
immunotherapy,
emerging
as
a
crucial
target
adjuvant
treatment
in
cancer
immunotherapy.
In
this
review,
we
discuss
molecular
cellular
basis
vascular
microenvironment-mediated
evasion
immune
responses
with
focus
on
vessel
abnormality,
dysfunctional
adhesion,
niche,
microenvironmental
stress
vasculature.
We
provide
overview
opportunities
challenges
related
these
mechanisms.
also
propose
genetic
programming
endothelial
cells
alternative
approach
recondition
overcome
Small,
Journal Year:
2020,
Volume and Issue:
16(21)
Published: March 12, 2020
Abstract
Metal
nanoparticles
(NPs)
are
frequently
encountered
in
daily
life,
and
concerns
have
been
raised
about
their
toxicity
safety.
Among
which,
they
naturally
accumulate
the
liver
after
introduction
into
body,
independent
of
route
administration.
Some
NPs
exhibit
intrinsic
pharmaceutical
effects
that
related
to
physical
parameters,
inadvertent
accumulation
can
exert
strong
on
function
structure.
Even
as
such
physiological
consequences
often
categorically
dismissed
toxic
deleterious,
there
cell
type‐specific
NP‐specific
biological
responses
elicit
distinctive
pharmacological
be
harnessed
for
good.
By
limiting
scope
discussion
metallic
NPs,
this
work
attempts
provide
a
balanced
perspective
safety
liver,
discusses
both
possible
therapeutic
benefits
potential
accidental
damage
arising
from
interaction
with
specific
parenchymal
nonparenchymal
types
liver.
Science Signaling,
Journal Year:
2020,
Volume and Issue:
13(635)
Published: June 9, 2020
Endothelial-to-mesenchymal
transition
(EndMT)
is
a
cellular
transdifferentiation
program
in
which
endothelial
cells
partially
lose
their
identity
and
acquire
mesenchymal-like
features.
Renal
capillary
can
undergo
EndMT
association
with
persistent
damage
of
the
renal
parenchyma.
The
functional
consequence(s)
kidney
fibrosis
remains
unexplored.
Here,
we
studied
effect
Twist
or
Snail
deficiency
on
fibrosis.
Conditional
deletion
Twist1
(which
encodes
Twist)
Snai1
Snail)
VE-cadherin+
Tie1+
inhibited
emergence
improved
two
different
injury/fibrosis
mouse
models.
Suppression
limited
peritubular
vascular
leakage,
reduced
tissue
hypoxia,
preserved
tubular
epithelial
health
function.
Hypoxia,
was
exacerbated
by
EndMT,
resulted
increased
Myc
abundance
cells,
enhanced
glycolysis,
suppression
fatty
acid
oxidation.
Pharmacological
epithelial-specific
genetic
ablation
ameliorated
restored
parenchymal
function
metabolic
homeostasis.
Together,
these
findings
demonstrate
role
for
response
to
injury
highlight
contribution
endothelial-epithelial
cross-talk
development
potential
therapeutic
intervention.
Journal of Oncology,
Journal Year:
2019,
Volume and Issue:
2019, P. 1 - 13
Published: Aug. 1, 2019
Cancer
cells
evolve
in
a
very
complex
tumor
microenvironment,
composed
of
several
cell
types,
among
which
the
endothelial
are
major
actors
angiogenesis.
Today,
these
also
characterized
for
their
plasticity,
as
have
demonstrated
potential
to
modify
phenotype
differentiate
into
mesenchymal
through
endothelial-to-mesenchymal
transition
(EndoMT).
This
cellular
plasticity
is
mediated
by
various
stimuli
including
transforming
growth
factor-
β
(TGF-
)
and
modulated
dependently
experimental
conditions.
Recently,
emerging
evidences
shown
that
EndoMT
involved
development
dissemination
cancer
escape
from
therapeutic
treatment.
In
this
review,
we
summarize
current
updates
on
its
main
induction
pathways.
addition,
discuss
role
tumorigenesis,
metastasis,
implication
therapy
resistance.
Journal of Experimental & Clinical Cancer Research,
Journal Year:
2020,
Volume and Issue:
39(1)
Published: June 17, 2020
Abstract
Background
Circular
RNAs
(circRNAs)
play
a
critical
regulatory
role
in
cancer
progression.
However,
the
underlying
mechanisms
of
circRNAs
hepatocellular
carcinoma
(HCC)
metastasis
remain
mostly
unknown.
Methods
Has_circ_0003998
(circ0003998)
was
identified
by
sequencing
HCC
patients
with
/without
portal
vein
tumor
thrombus
(PVTT)
metastasis.
The
expression
level
circ0003998
further
detected
situ
hybridization
on
tissues
microarray
(ISH-TMA)
and
qRT-PCR
25
PVTT
Moreover,
50
without
were
recruited
together
to
analyze
correlation
between
clinical
characteristics.
Transwell,
migration
CCK8
assays,
as
well
nude
mice
model
lung
or
liver
used
evaluate
epithelial
mesenchymal
transition
(EMT)
HCC.
miR-143-3p
PCBP1
determined
dual-luciferase
reporter
assay,
nuclear-cytoplasmic
fractionation,
fluorescent
hybridization,
RNA
pull-
down,
microRNA
sequence,
western
blot
immunoprecipitation.
Results
Compared
adjacent
normal
(ANL),
significantly
upregulated
tissues,
its
correlates
aggressive
characteristics
patients.
Further
assays
suggested
that
promoted
EMT
both
vitro
vivo.
Mechanistically,
our
data
indicated
may
act
ceRNA
(competing
endogenous
RNA)
microRNA-143-3p
relieve
repressive
effect
EMT-related
stimulator,
FOSL2;
meanwhile,
could
bind
PCBP1-poly(rC)
binding
protein
1
(PCBP1)
increase
genes,
CD44v6.
Conclusion
Circ0003998
promotes
circ0003998/miR-143-3p/FOSL2
axis
/PCBP1/CD44v6
axis.
Frontiers in Immunology,
Journal Year:
2021,
Volume and Issue:
12
Published: Dec. 20, 2021
Immunotherapy
holds
great
promise
for
treating
cancer.
Nonetheless,
T
cell-based
immunotherapy
of
solid
tumors
has
remained
challenging,
largely
due
to
the
lack
universal
tumor-specific
antigens
and
an
immunosuppressive
tumor
microenvironment
(TME)
that
inhibits
lymphocyte
infiltration
activation.
Aberrant
vascularity
characterizes
malignant
tumors,
which
fuels
formation
immune-hostile
induces
resistance
immunotherapy,
emerging
as
a
crucial
target
adjuvant
treatment
in
cancer
immunotherapy.
In
this
review,
we
discuss
molecular
cellular
basis
vascular
microenvironment-mediated
evasion
immune
responses
with
focus
on
vessel
abnormality,
dysfunctional
adhesion,
niche,
microenvironmental
stress
vasculature.
We
provide
overview
opportunities
challenges
related
these
mechanisms.
also
propose
genetic
programming
endothelial
cells
alternative
approach
recondition
overcome
