The Journal of Physiological Sciences,
Journal Year:
2023,
Volume and Issue:
73(1)
Published: Nov. 15, 2023
Physiological
roles
of
Cl-,
a
major
anion
in
the
body,
are
not
well
known
compared
with
those
cations.
This
review
article
introduces:
(1)
Cl-
bodily
and
cellular
functions;
(2)
range
cytosolic
concentration
([Cl-]c);
(3)
whether
[Cl-]c
could
change
cell
volume
under
an
isosmotic
condition;
(4)
conditions
where
multiple
transporters
channels
contribute
to
influx
efflux
state;
(5)
be
large
enough
act
as
signals;
(6)
effects
on
cytoskeletal
tubulin
polymerization
through
inhibition
GTPase
activity
polymerization-dependent
biological
activity;
(7)
proliferation;
(8)
Cl--regulatory
mechanisms
ciliary
motility;
(9)
sweet/umami
taste
receptors;
(10)
with-no-lysine
kinase
(WNK);
(11)
regulation
epithelial
Na+
transport;
(12)
relationship
between
H+
body
functions.
Journal of drug targeting,
Journal Year:
2025,
Volume and Issue:
unknown, P. 1 - 33
Published: Jan. 15, 2025
The
lung
tumor
microenvironment
is
composed
of
various
cell
types,
including
cancer
cells,
stromal
and
immune
as
well
extracellular
matrix
(ECM).
These
cells
surrounding
ECM
create
a
stiff,
hypoxic,
acidic,
immunosuppressive
that
can
augment
the
resistance
tumors
to
different
forms
death
facilitate
invasion
metastasis.
This
environment
induce
chemo/radiotherapy
by
inducing
anti-apoptosis
mediators
such
phosphoinositide
3-kinase
(PI3K)/Akt,
signal
transducer
activator
transcription
3
(STAT3),
nuclear
factor
κB
(NF-κB),
leading
exhaustion
antitumor
immunity
further
chemo/radiotherapy.
In
addition,
resist
boosting
multidrug
mechanisms
antioxidant
defense
systems
within
other
TME
components.
this
review,
we
discuss
interactions
communications
between
these
components
also
effects
hypoxia,
evasion,
remodeling
on
resistance.
Finally,
review
current
strategies
in
preclinical
clinical
studies,
inhibition
checkpoint
molecules,
chemoattractants,
cytokines,
growth
factors,
programmed
1
(PD-1),
insulin-like
2
(IGF-2)
for
targeting
overcome
chemotherapy
radiotherapy.
Cancer Immunology Immunotherapy,
Journal Year:
2024,
Volume and Issue:
73(2)
Published: Jan. 27, 2024
Macrophages
constitute
a
major
part
of
tumor
microenvironment,
and
most
existing
data
demonstrate
their
ruling
role
in
the
development
anti-drug
resistance
cancer
cell.
One
powerful
protection
system
is
based
on
heat
shock
proteins
whose
synthesis
triggered
by
activated
Heat
Shock
Factor-1
(HSF1);
inhibition
HSF1
with
CL-43
sensitized
A549
lung
cells
to
anti-cancer
effect
etoposide.
Notably,
analyzing
xenografts
mice
we
observed
nest-like
pattern
co-localization
demonstrating
enhanced
expression
macrophages,
decided
check
whether
above
arrangement
has
functional
value
for
both
cell
types.
It
was
found
that
incubation
or
DLD1
colon
either
human
monocytes
THP1
monocyte-like
increased
Importantly,
same
shown
when
primary
cultures
tumors
were
incubated
monocytes.
To
prove
implicated
caused
monocytic
cells,
generated
an
subline
devoid
which
did
not
respond
cells.
The
pharmacological
also
abolished
highlighting
new
target
tumor-associated
macrophages
proteostasis
mechanism.
We
have
developed
an
innovative
Cu-doped
and
DTX-loaded
Cu-MnO2@DTX@FA
(MCDF)
nanodrug
designed
to
strategically
alter
tumor
microenvironment
(TME)
by
harnessing
the
synergistic
effects
of
chemodynamic
therapy
(CDT),
chemotherapeutic
agents,
induction
ferroptosis
cuproptosis.
The
MCDF
efficiently
degrades,
releasing
abundant
Mn4+,
Cu2+,
DTX.
conversion
Cu2+
Cu+
facilitated
FDX1
initiates
cuproptosis,
while,
similar
Mn2+,
reacts
with
hydrogen
peroxide
(H2O2)
generate
hydroxyl
radicals
(·OH).
Mn4+
oxidize
glutathione
(GSH),
significantly
depleting
GSH
levels
in
cells
inactivating
GPX4,
which
further
promotes
ferroptosis.
release
intensifies
DTX
effectively
disrupts
cell
division
cycle,
thereby
inhibiting
proliferation
spread
cells.
FA-modified
is
evade
immune
detection
while
selectively
targeting
tissues,
ensuring
precision
treatment
delivery.
This
cutting-edge
material
not
only
provides
a
multifunctional
therapeutic
strategy
but
also
sets
stage
for
next
generation
tumor-targeting
nanomedicines.
