Journal of Ethnopharmacology,
Journal Year:
2024,
Volume and Issue:
326, P. 117995 - 117995
Published: Feb. 28, 2024
Inflammatory
bowel
disease
(IBD)
presents
a
risk
of
carcinogenesis,
which
escalates
with
the
duration
IBD.
Persistent
histological
inflammation
is
considered
to
be
driving
factor
colitis
carcinogenesis.
Effective
control
helpful
prevent
and
treat
colitis-related
colorectal
cancer
(CAC).
Anchang
Yuyang
Decoction
(AYD),
traditional
Chinese
medicine
(TCM)
formula,
originated
from
ancient
prescription
TCM
for
treating
cancer.
AYD
has
demonstrated
efficacy
in
IBD
potential
anti-carcinogenic
properties.
Archives of Toxicology,
Journal Year:
2024,
Volume and Issue:
98(5), P. 1241 - 1252
Published: March 13, 2024
Abstract
Per-
and
polyfluoroalkyl
substances
(PFAS)
are
a
large
group
of
synthetic
persistent
chemicals,
which
used
in
many
industrial
commercial
applications.
Hundreds
different
PFAS
have
been
identified
the
environment
they
commonly
found
also
human
blood.
Due
to
chemical
stability
extensive
use,
pose
risk
for
health
wildlife.
Mounting
evidence
indicates
that
PFAS-exposure
adversely
affects
organs
including
liver,
kidney,
reproductive
tissues
induces
tumors
laboratory
rodents.
Epidemiological
studies
show
association
between
some
humans.
Effects
complex
obviously
do
not
depend
only
on
concentration
structure
PFAS,
but
age
sex
exposed
individuals.
It
has
difficult
causal
link
tumors.
Moreover,
molecular
mechanisms
effects
poorly
understood.
directly
mutagenic
induce
formation
DNA
binding
metabolites,
thus
assumed
act
more
through
non-genotoxic
mechanisms.
In
this
review,
we
discuss
involvement
PFAS-compounds
tumor
development
where
exposure
associated
with
cancer
epidemiological
animal
(liver,
testicle
breast).
We
will
focus
pathways
related
following
PFAS-exposure.
International Journal of Molecular Sciences,
Journal Year:
2025,
Volume and Issue:
26(2), P. 736 - 736
Published: Jan. 16, 2025
Peroxisome
proliferator-activated
receptors
(PPARs)
are
considered
good
drug
targets
for
breast
cancer
because
of
their
involvement
in
fatty
acid
metabolism
that
induces
cell
proliferation.
In
this
study,
we
used
the
KAIMRC1
line.
We
showed
PPARE-Luciferase
reporter
gets
highly
activated
without
adding
any
exogenous
ligand
when
PPAR
alpha
is
co-transfected,
and
antagonist
GW6471
can
inhibit
activity.
Using
system,
screened
240
compounds
representing
kinase
inhibitors,
epigenetic
modulators,
stem
differentiators
identified
PPARα-activated
cell.
selected
11
(five
two
differentiators,
four
inhibitors)
inhibited
by
at
least
40%
compared
to
controls
(DMSO-treated
cells).
tested
them
a
dose-dependent
manner
measured
viability
after
48
h.
All
induced
killing
different
IC50
values.
compounds,
PHA665752
NSC3852,
dissect
how
they
kill
cells
GW6741.
First,
molecular
docking
TR-FRET
PPARα
binding
assay
GW6471,
these
could
not
bind
PPARα.
This
means
pathway
independently
rather
than
receptor.
further
confirmed
NSC3852
induce
depending
on
level
expression,
as
such,
potency
SW620
colon
line
expresses
lowest
was
less
potent
MDA-MB-231
lines.
Further,
using
an
apoptosis
array
gene
expression
panel,
found
both
regulate
controlling
genes
involved
oxidation
process.
Our
findings
suggest
have
opposite
effects
involving
Although
do
fully
understand
mechanism
action,
our
data
provide
new
insights
into
potential
role
targeting
cells.
Cells,
Journal Year:
2022,
Volume and Issue:
11(20), P. 3215 - 3215
Published: Oct. 13, 2022
Peroxisome
proliferator-activated
receptor-γ
(PPAR-γ)
has
emerged
as
one
of
the
most
extensively
studied
transcription
factors
since
its
discovery
in
1990,
highlighting
importance
etiology
and
treatment
numerous
diseases
involving
various
types
cancer,
type
2
diabetes
mellitus,
autoimmune,
dermatological
cardiovascular
disorders.
Ligands
are
regarded
key
determinant
for
tissue-specific
activation
PPAR-γ.
However,
mechanism
governing
this
process
is
merely
a
contradictory
debate
which
yet
to
be
systematically
researched.
Either
these
receptors
get
weakly
activated
by
endogenous
or
natural
ligands
leads
direct
over-activation
synthetic
ligands,
serving
complete
full
agonists.
Therefore,
fine-tuning
on
action
PPAR-γ
more
subtle
modulation
can
rewarding
approach
might
open
new
avenues
several
diseases.
In
recent
era,
researchers
have
sought
develop
safer
partial
agonists
order
dodge
toxicity
induced
agonists,
akin
balanced
activation.
With
particular
reference
review
concentrates
therapeutic
role
especially
cancer
treatment.
Additionally,
timely
examination
their
efficacy
other
disease-fate
decisions
been
also
discussed.
Biomolecules,
Journal Year:
2024,
Volume and Issue:
14(6), P. 728 - 728
Published: June 19, 2024
Peroxisome
proliferator-activated
receptor
gamma
(PPARγ)
is
a
transcription
factor
expressed
in
many
tissues,
including
skin,
where
it
essential
for
maintaining
skin
barrier
permeability,
regulating
cell
proliferation/differentiation,
and
modulating
antioxidant
inflammatory
responses
upon
ligand
binding.
Therefore,
PPARγ
activation
has
important
implications
homeostasis.
Over
the
past
20
years,
with
increasing
interest
role
of
PPARs
physiopathology,
considerable
effort
been
devoted
to
development
ligands
as
therapeutic
option
disorders.
In
addition,
also
regulates
sebocyte
differentiation
lipid
production,
making
potential
target
sebaceous
disorders
such
acne.
A
large
number
studies
suggest
that
acts
tumor
suppressor
both
melanoma
non-melanoma
cancers,
but
its
tumorigenesis
remains
controversial.
this
review,
we
have
summarized
current
state
research
into
health
disease
how
may
provide
starting
point
more
potent
selective
low
toxicity
profile,
thereby
reducing
unwanted
side
effects.
Cells,
Journal Year:
2024,
Volume and Issue:
13(13), P. 1081 - 1081
Published: June 22, 2024
Successful
pregnancy
depends
on
precise
molecular
regulation
of
uterine
physiology,
especially
during
the
menstrual
cycle.
Deregulated
oxidative
stress
(OS),
often
influenced
by
inflammatory
changes
but
also
environmental
factors,
represents
a
constant
threat
to
this
delicate
balance.
Oxidative
induces
reciprocally
regulated
nuclear
factor
erythroid
2-related
2/peroxisome
proliferator-activated
receptor-gamma
(Nrf2/PPARγ)
pathway.
However,
increased
PPARγ
activity
appears
be
double-edged
sword
in
endometrial
physiology.
Activated
attenuates
inflammation
and
OS
restore
redox
homeostasis.
it
interferes
with
physiological
processes
cycle,
such
as
hormonal
signaling
angiogenesis.
This
review
provides
an
elucidation
mechanisms
that
support
interplay
between
OS.
Additionally,
offers
fresh
perspectives
Nrf2/PPARγ
pathway
concerning
receptivity
its
potential
implications
for
infertility.
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(2), P. 1316 - 1316
Published: Jan. 10, 2023
The
NF-E2-related
factor
2
transcription
(Nrf2)
orchestrates
the
basal
and
stress-inducible
activation
of
a
vast
array
antioxidant
genes.
A
high
amount
reactive
oxygen
species
(ROS)
promotes
carcinogenesis
in
cells
with
defective
redox-sensitive
signaling
factors
such
as
Nrf2.
In
breast
cancer
(BC),
emerging
evidence
indicates
that
increased
Nrf2
activity
enhances
cell
metastatic
potential.
An
interconnection
between
peroxisome
proliferator-activated
receptors
(PPARs)
pathways
has
been
shown.
this
light,
newly
synthesized
PPARα
antagonists,
namely
IB42,
IB44,
IB66,
were
tested
BC
line
MCF7
parallel
GW6471
reference
compound.
Our
results
show
most
promising
compound
phenylsulfonimide
series
(IB66)
is
able
to
decrease
proliferation
by
blocking
at
G2/M
checkpoint.
underlying
mechanism
investigated,
disclosing
caspase
3/Akt-dependent
apoptotic/pyroptotic
pathway
induced
generation
oxidative
stress.
Moreover,
involvement
COX2
IB66-treated
response
highlighted.
reported
data
lay
groundwork
for
development
alternative
targeted
therapy
involving
Nrf2/PPARα
molecular
axis,
overcome
chemoresistance
cause
better
clinical
outcomes,
promoting
other
forms
programmed
death,
pyroptosis.
Saudi Pharmaceutical Journal,
Journal Year:
2024,
Volume and Issue:
32(5), P. 102059 - 102059
Published: April 1, 2024
Peroxisome
proliferator-activated
receptor-gamma
(PPARγ)
has
been
recently
shown
to
play
a
role
in
many
cancers.
The
breast
tissue
of
triple-negative
cancer
(TNBC)
patients
were
found
have
significantly
lower
expression
PPARγ
than
the
other
subtypes.
Furthermore,
activation
was
exert
anti-tumor
effects
by
inhibiting
cell
proliferation,
differentiation,
growth,
cycle,
and
inducing
apoptosis.
To
start
with,
we
performed
bioinformatic
analysis
data
from
OncoDB,
which
showed
pattern
different
types.
In
addition,
high
associated
with
better
patient
survival.
Therefore,
tested
impact
pioglitazone,
ligand,
on
cytotoxic
activity
cisplatin
TNBC
line.
MDA-MB-231
cells
treated
either
(40
μM)
or
without
pioglitazone
(30
60
for
72
h.
MTT
results
significant
dose-dependent
decrease
viability
as
result
using
combination
compared
alone.
protein
Bcl-2,
known
antiapoptotic
marker,
decreased
at
doses
40
30
μM,
respectively.
On
hand,
cleaved-
poly-ADP
ribose
polymerase
(PARP)
-caspase-9,
are
pro-apoptotic
markers,
upregulated
group
solo
treatments.
Taken
together,
addition
further
reduced
enhanced
apoptosis
chemotherapy
