The Journal of Steroid Biochemistry and Molecular Biology,
Journal Year:
2024,
Volume and Issue:
241, P. 106520 - 106520
Published: April 13, 2024
Gonadal
hormone
deprivation
(GHD)
and
decline
such
as
menopause
bilateral
oophorectomy
are
associated
with
an
increased
risk
of
neurodegeneration.
Yet,
therapies
(HTs)
show
varying
efficacy,
influenced
by
factors
sex,
drug
type,
timing
treatment
relative
to
decline.
We
hypothesize
that
the
molecular
environment
brain
undergoes
a
transition
following
GHD,
impacting
effectiveness
HTs.
Using
GHD
model
in
mice
treated
Tibolone,
we
conducted
proteomic
analysis
identified
reprogrammed
response
compound
stimulates
estrogenic,
progestogenic,
androgenic
pathways.
Through
comprehensive
network
pharmacological
workflow,
particularly
within
"Pathways
Neurodegeneration",
well
interconnected
pathways
including
"cellular
respiration",
"carbon
metabolism",
homeostasis".
Analysis
revealed
23
proteins
whose
Tibolone
depended
on
and/or
implicating
critical
processes
like
oxidative
phosphorylation
calcium
signalling.
Our
findings
suggest
therapeutic
efficacy
HTs
may
depend
these
variables,
suggesting
need
for
greater
precision
medicine
considerations
whilst
highlighting
uncover
underlying
mechanisms.
Journal of Advanced Research,
Journal Year:
2023,
Volume and Issue:
54, P. 271 - 292
Published: Feb. 14, 2023
Triple-negative
breast
cancer
(TNBC)
is
a
heterogeneous,
aggressive
phenotype
of
with
associated
chemoresistance.
The
development
chemo-
or
radioresistance
could
be
attributed
to
diverse
tumor
microenvironments,
overexpression
membrane
proteins
(transporters),
epigenetic
changes,
and
alteration
the
cell
signaling
pathways/genes
stem
cells
(CSCs).
Due
heterogeneous
nature
TNBC,
therapeutic
response
existing
modalities
offers
limited
scope
thus
results
in
reccurance
after
therapy.
To
establish
landmark
efficacy,
number
novel
have
been
proposed.
In
addition,
reversal
resistance
that
developed
during
treatment
may
altered
by
employing
appropriate
modalities.
This
review
aims
discuss
plethora
investigations
carried
out,
which
will
help
readers
understand
make
an
choice
therapy
directed
toward
complete
elimination
TNBC.
manuscript
addresses
major
contributory
factors
from
microenvironment
are
responsible
for
chemoresistance
poor
prognosis.
cellular
events
molecular
mechanism-based
interventions
explained
detail.
Inhibition
ABC
transporters,
pathways
CSCs,
modification
promising
this
regard.
TNBC
progression,
invasion,
metastasis
recurrence
can
also
inhibited
blocking
multiple
pathways,
targeting
specific
receptors/epigenetic
targets,
disrupting
bioenergetics
generating
reactive
oxygen
species
(ROS).
Military Medical Research,
Journal Year:
2025,
Volume and Issue:
12(1)
Published: Feb. 11, 2025
Abstract
Cancer
recurrence,
driven
by
the
phenomenon
of
tumor
dormancy,
presents
a
formidable
challenge
in
oncology.
Dormant
cancer
cells
have
ability
to
evade
detection
and
treatment,
leading
relapse.
This
review
emphasizes
urgent
need
comprehend
dormancy
its
implications
for
recurrence.
Despite
notable
advancements,
significant
gaps
remain
our
understanding
mechanisms
underlying
lack
reliable
biomarkers
predicting
provides
comprehensive
analysis
cellular,
angiogenic,
immunological
aspects
dormancy.
It
highlights
current
therapeutic
strategies
targeting
dormant
cells,
particularly
combination
therapies
immunotherapies,
which
hold
promise
preventing
By
elucidating
these
proposing
innovative
research
methodologies,
this
aims
deepen
ultimately
facilitating
development
more
effective
recurrence
improving
patient
outcomes.
Frontiers in Molecular Biosciences,
Journal Year:
2022,
Volume and Issue:
9
Published: Aug. 29, 2022
The
Golgi-sialyltransferase
ST6Gal1
(βgalactosidase
α2,6
sialyltransferase
1),
adds
the
negatively
charged
sugar,
sialic
acid,
to
terminal
galactose
of
N-glycosylated
proteins.
Upregulation
is
observed
in
many
malignancies,
and
a
large
body
research
has
determined
that
ST6Gal1-mediated
sialylation
impacts
cancer
hallmarks.
affects
oncogenic
behaviors
including
sustained
proliferation,
enhanced
self-renewal,
epithelial-to-mesenchymal
transition,
invasion,
chemoresistance.
However,
there
are
relatively
few
ST6GaL1
related
signaling
pathways
well-established
mediate
these
biologies:
greater
delineation
specific
targets
mechanisms
orchestrated
by
needed.
aim
this
review
provide
summary
our
current
understanding
select
affected
ST6Gal1.
Frontiers in Oncology,
Journal Year:
2023,
Volume and Issue:
13
Published: July 21, 2023
Hepatocellular
carcinoma
(HCC)
is
one
of
the
deadliest
cancers
due
to
multifocal
development
and
distant
metastasis
resulting
from
late
diagnosis.
Consequently,
new
approaches
HCC
diagnosis
treatment
are
required
reduce
mortality
rates.
A
large
body
evidence
suggests
that
non-coding
RNAs
(ncRNAs)
important
in
cancer
initiation
progression.
Cancer
cells
release
many
these
ncRNAs
into
blood
or
urine,
enabling
their
use
as
a
diagnostic
tool.
Circular
(CircRNAs)
members
regulate
cell
expansion,
migration,
metastasis,
chemoresistance
through
different
mechanisms
such
Wnt/β-catenin
Signaling
pathway.
The
pathway
plays
prominent
roles
several
biological
processes
including
organogenesis,
stem
regeneration,
survival.
Aberrant
signaling
both
pathways
mentioned
above
could
affect
progression
cancers,
HCC.
Based
on
studies
investigated
current
review,
circRNAs
have
an
effect
formation
by
sponging
miRNAs
RNA-binding
proteins
(RBPs)
regulating
Therefore,
circRNAs/miRNAs
RBPs/Wnt/β-catenin
be
considered
promising
prognostic
therapeutic
targets
ACS Pharmacology & Translational Science,
Journal Year:
2023,
Volume and Issue:
6(5), P. 671 - 682
Published: April 21, 2023
Breast
cancer
is
one
of
the
most
common
cancers
in
women
worldwide,
yet
conventional
treatments
have
several
shortcomings,
including
low
specificity,
systemic
toxicity,
and
drug
resistance.
Nanomedicine
technologies
provide
a
promising
alternative
while
also
overcoming
limitations
posed
by
therapies.
This
mini-Review
highlights
important
signaling
pathways
related
to
occurrence
development
breast
current
therapies,
followed
an
analysis
various
nanomedicine
developed
for
diagnosis
treatment
cancers.
Cell Regeneration,
Journal Year:
2021,
Volume and Issue:
10(1)
Published: April 1, 2021
Abstract
Regeneration
is
an
evolutionarily
conserved
process
in
animal
kingdoms,
however,
the
regenerative
capacities
differ
from
species
and
organ/tissues.
Mammals
possess
very
limited
potential
to
replace
damaged
organs,
whereas
non-mammalian
usually
have
impressive
abilities
regenerate
organs.
The
regeneration
requires
proper
spatiotemporal
regulation
key
signaling
pathways.
canonical
Notch
Wnt
pathways,
two
fundamental
signals
guiding
development,
been
demonstrated
play
significant
roles
of
vertebrates.
In
recent
years,
increasing
evidence
has
implicated
cross-talking
between
during
organ
regeneration.
this
review,
we
summarize
several
representative
events,
emphasizing
functions
molecular
bases
their
interplay
these
processes,
shedding
light
on
utilizing
pathways
enhance
mammals
design
legitimate
therapeutic
strategies.
Genes,
Journal Year:
2022,
Volume and Issue:
13(1), P. 138 - 138
Published: Jan. 13, 2022
The
Wnt
pathway
is
involved
in
several
processes
essential
for
bone
development
and
homeostasis.
For
proper
functioning,
the
tightly
regulated
by
numerous
extracellular
elements
that
act
both
activating
inhibiting
at
different
moments.
This
review
aims
to
describe,
summarize
update
findings
regarding
modulators
of
pathway,
including
co-receptors,
ligands
inhibitors,
relation
homeostasis,
with
an
emphasis
on
animal
models
generated,
diseases
associated
each
gene
which
member
involved.
precise
knowledge
all
these
will
help
us
identify
possible
targets
can
be
used
as
a
therapeutic
target
treatment
such
osteoporosis.
Current Issues in Molecular Biology,
Journal Year:
2023,
Volume and Issue:
45(1), P. 434 - 464
Published: Jan. 5, 2023
The
transcriptomic
analysis
of
microarray
and
RNA-Seq
datasets
followed
our
own
bioinformatic
pipeline
to
identify
a
transcriptional
regulatory
network
lung
cancer.
Twenty-six
transcription
factors
are
dysregulated
co-expressed
in
most
the
cancer
pulmonary
arterial
hypertension
datasets,
which
makes
them
frequently
factors.
Co-expression,
gene
regulatory,
coregulatory,
networks,
along
with
fibration
symmetries,
were
constructed
common
connection
patterns,
alignments,
main
regulators,
target
genes
order
analyze
factor
complex
formation,
as
well
its
synchronized
co-expression
patterns
every
type
function
over
deregulated
was
validated
ChEA3
enrichment
analysis.
A
Kaplan-Meier
plotter
linked
dysregulation
top
patients'
survival.
Our
results
indicate
that
has
unique
hypertension,
regulated
coordinated
cooperative
manner
by
might
be
associated
critical
biological
processes
signaling
pathways
related
acquisition
hallmarks
cancer,
making
potentially
relevant
tumor
biomarkers
for
early
diagnosis
targets
development
personalized
therapies
against
International Journal of Medical Sciences,
Journal Year:
2021,
Volume and Issue:
18(6), P. 1442 - 1448
Published: Jan. 1, 2021
Activating
transcription
factor
4
(ATF4)
is
a
member
of
the
cAMP
response
element
binding
(CREB)
protein
family
and
has
been
reported
to
participate
in
cancer
progression;
however,
its
molecular
mechanism
not
fully
understood.In
this
study,
we
investigated
function
ATF4
non-small
cell
lung
regulation.We
detected
cytoplasmic
nuclear
expression
A549,
H1299,
LK2
cells,
total
was
higher
than
that
HBE
cells
(p
<
0.05).Higher
all
these
compared
0.05).Overexpression
A549
significantly
promoted
growth
invasion
0.05).Expression
Wnt
signaling
molecules,
including
β-catenin,
MMP7,
cyclin
D1,
activity
canonical
were
also
by
0.05).ICG001,
inhibitor
selectively
inhibits
β-catenin/
cyclic
adenosine
monophosphate
(CBP)
interaction,
inhibited
signaling.The
ICG001
0.05).However,
treatment
with
ICG001,
ability
treated
both
cDNA
increased
0.05),
which
indicates
dependent
only
on
Wnt/β-catenin
regulation
β-catenin
affected
>
0.05).The
promote
abolished
0.05).These
results
indicate
may
contribute
progression
at
least
partly
regulating
signaling.
Cells,
Journal Year:
2024,
Volume and Issue:
13(11), P. 897 - 897
Published: May 23, 2024
Glioblastoma
Multiforme
(GBM)
is
an
aggressive
brain
tumor
with
a
high
mortality
rate.
Direct
reprogramming
of
glial
cells
to
different
cell
lineages,
such
as
induced
neural
stem
(iNSCs)
and
neurons
(iNeurons),
provides
genetic
tools
manipulate
cell’s
fate
potential
therapy
for
neurological
diseases.
NeuroD1
(ND1)
master
transcriptional
factor
neurogenesis
it
promotes
neuronal
differentiation.
In
the
present
study,
we
tested
hypothesis
that
expression
ND1
in
GBM
can
force
them
differentiate
toward
post-mitotic
halt
progression.
cultured
human
lines,
including
LN229,
U87,
U373
temozolomide
(TMZ)-sensitive
T98G
TMZ-resistant
cells,
lineage
conversion
was
by
adeno-associated
virus
(AAV)
package
carrying
ND1.
Twenty-one
days
after
AAV-ND1
transduction,
ND1-expressing
displayed
markers
MAP2,
TUJ1,
NeuN.
The
ND1-induced
transdifferentiation
regulated
Wnt
signaling
markedly
enhanced
under
hypoxic
condition
(2%
O2
vs.
21%
O2).
cultures
had
fewer
BrdU-positive
proliferating
compared
vector
control
cultures.
Increased
death
visualized
TUNEL
staining,
reduced
migrative
activity
demonstrated
wound-healing
test
both
TMZ-sensitive
-resistant
cells.
striking
contrast
cancer
converted
expressed
anti-tumor
gene
p53.
orthotopical
mouse
model,
AAV-ND1-reprogrammed
were
transplanted
into
fornix
cyclosporine-immunocompromised
C57BL/6
brain.
Compared
cell-formed
tumors,
from
ND1-reprogrammed
formed
smaller
tumors
TUJ1
Thus,
using
single-factor
overcame
drug
resistance,
converting
malignant
heterogeneous
normal
neuron-like
vitro
vivo.
These
novel
observations
warrant
further
research
patient-derived
xenograft
(PDX)
models
potentially
effective
treatment
deadly
likely
other
astrocytoma
tumors.