Clinical and Translational Medicine,
Год журнала:
2024,
Номер
14(1)
Опубликована: Янв. 1, 2024
Abstract
Background
Prostate
cancer
(PCa)
initially
shows
satisfactory
response
to
therapies
targeting
the
androgen
receptor
(AR).
However,
progression
a
castration‐resistant
stage
indicates
poor
prognosis
in
PCa
patients.
AR
signalling
still
plays
central
role
most
prostate
cancers
(CRPC).
Therefore,
unveiling
mechanisms
of
reactivation
under
androgen‐deprived
conditions
is
imperative
discover
novel
therapeutic
targets
for
CRPC.
Methods
Using
an
integrative
analysis
transcriptomics
three
independent
cohorts
and
published
landscape
AR‐regulated
long
non‐coding
RNA
(lncRNA),
lncRNA
LINC01126
was
selected
as
candidate
gene
that
could
drive
CRPC
further
study.
Quantitative
reverse
transcription
polymerase
chain
reaction,
situ
hybridisation
(ISH)
fluorescent
ISH
were
performed
detect
tissues
cells.
The
functional
mechanism
investigated
using
vitro
vivo
gain
loss
function
assays.
Results
LINC01126,
identified
AR‐repressed
lncRNA,
significantly
upregulated
after
AR‐targeted
therapies.
In
addition,
we
found
associated
with
prognosis.
We
also
proved
stabilised
protein
enhanced
nuclear
translocation
transactivation
by
promoting
transition
from
O‐GlcNAcylation
at
threonine
80
phosphorylation
serine
81
(S81)
within
protein.
Mechanism
revealed
facilitates
interaction
CDK9
impedes
binding
O‐linked
N‐acetylglucosamine
(O‐GlcNAc)
transferase
AR.
Consequently,
expression
sufficient
activate
without
androgen.
overexpression
increased,
whereas
knockdown
decreased
castration
resistance
traits
cells
vivo.
Furthermore,
our
data
showed
LINC01126‐targeting
antisense
oligonucleotides
(ASO)
substantially
inhibited
vitro.
Conclusions
Our
research
expands
functions
sustaining
androgen‐independent
activity
reveals
may
be
new
target
PCa.
Biomedicine & Pharmacotherapy,
Год журнала:
2022,
Номер
155, С. 113774 - 113774
Опубликована: Окт. 3, 2022
One
of
the
malignant
tumors
in
women
that
has
involved
both
developed
and
developing
countries
is
breast
cancer.
Similar
to
other
types
tumors,
cancer
cells
demonstrate
high
metastatic
nature.
Besides,
tumor
have
ability
drug
resistance.
EMT
related
mechanism
metastasis
focus
current
manuscript
highlighting
function
malignancy
Breast
increase
their
migration
by
induction
During
EMT,
N-cadherin
vimentin
levels
increase,
E-cadherin
decrease
mediate
EMT-induced
invasion.
Different
kinds
anti-cancer
agents
such
as
tamoxifen,
cisplatin
paclitaxel
mediates
chemoresistance
feature
cells.
Furthermore,
correlates
with
radio-resistance
tumor.
Clinical
aspect
reversing
preventing
chemotherapy
or
radiotherapy
failure
patients
improving
survival
time.
The
anti-tumor
suppress
can
be
used
for
decreasing
invasion
increasing
chemosensitivity
lncRNAs,
miRNAs
factors
modulate
progression
are
discussed
here.
Biomedicine & Pharmacotherapy,
Год журнала:
2023,
Номер
158, С. 114204 - 114204
Опубликована: Янв. 4, 2023
Glioblastoma
(GBM)
is
one
of
the
most
malignant
cancers
central
nervous
system
and
due
to
its
sensitive
location,
surgical
resection
has
high
risk
therefore,
chemotherapy
radiotherapy
are
utilized
for
treatment.
However,
chemoresistance
radio-resistance
other
problems
in
GBM
Hence,
new
therapies
based
on
genes
recommended
treatment
GBM.
PTEN
a
tumor-suppressor
operator
cancer
that
inhibits
PI3K/Akt/mTOR
axis
diminishing
growth,
metastasis
drug
resistance.
In
current
review,
function
PTEN/PI3K/Akt
progression
evaluated.
Mutation
or
depletion
leads
increase
progression.
Low
expression
level
mediates
poor
prognosis
by
increasing
proliferation
invasion,
promotes
malignancy
tumor
cells.
Moreover,
loss
signaling
can
result
therapy
resistance
Activation
impairs
metabolism
via
glycolysis
inhibition.
contrast
PTEN,
PI3K/Akt
oncogenic
during
progression,
enhances.
shows
positive
association
with
pathways
similar
signaling,
regulated
non-coding
RNAs.
upregulation
inhibition
anti-cancer
agents
be
beneficial
interfering
This
review
emphasizes
networks
related
provides
insights
targeting
this
effective
Biomedicine & Pharmacotherapy,
Год журнала:
2023,
Номер
160, С. 114392 - 114392
Опубликована: Фев. 15, 2023
Prostate
cancer
is
among
most
malignant
tumors
around
the
world
and
this
urological
tumor
can
be
developed
as
result
of
genomic
mutations
their
accumulation
during
progression
towards
advanced
stage.
Due
to
lack
specific
symptoms
in
early
stages
prostate
cancer,
patients
are
diagnosed
that
cells
display
low
response
chemotherapy.
Furthermore,
enhance
aggressiveness
cells.
Docetaxel
paclitaxel
suggested
well-known
compounds
for
chemotherapy
they
possess
a
similar
function
therapy
based
on
inhibiting
depolymerization
microtubules,
impairing
balance
microtubules
subsequent
delay
cell
cycle
progression.
The
aim
current
review
highlight
mechanisms
docetaxel
resistance
cancer.
When
oncogenic
factors
such
CD133
upregulation
PTEN
tumor-suppressor
shows
decrease
expression,
malignancy
enhances
induce
drug
resistance.
phytochemicals
anti-tumor
have
been
utilized
suppressing
chemoresistance
Naringenin
lovastatin
used
enhancing
sensitivity.
Moreover,
nanostructures
polymeric
micelles
nanobubbles
delivery
decreasing
risk
development.
These
subjects
highlighted
provide
new
insight
reversing
Biomedicine & Pharmacotherapy,
Год журнала:
2022,
Номер
154, С. 113609 - 113609
Опубликована: Авг. 27, 2022
Epigenetic
factors
are
critical
regulators
of
biological
and
pathological
mechanisms
they
could
interact
with
different
molecular
pathways.
Targeting
epigenetic
has
been
an
idea
approach
in
disease
therapy,
especially
cancer.
Accumulating
evidence
highlighted
function
long
non-coding
RNAs
(lncRNAs)
as
cancer
initiation
development
focused
on
their
association
downstream
targets.
microRNAs
(miRNAs)
the
most
well-known
targets
lncRNAs
present
review
focuses
lncRNA-miRNA
axis
malignancy
therapy
resistance
tumors.
LncRNA-miRNA
regulates
cell
death
such
apoptosis
autophagy
cancers.
This
affects
tumor
metastasis
via
regulating
EMT
MMPs.
Besides,
determines
sensitivity
cells
to
chemotherapy,
radiotherapy
immunotherapy.
Based
studies,
can
be
affected
by
drugs
genetic
tools
this
may
affect
expression
level
miRNAs
targets,
leading
suppression/progression.
LncRNAs
have
both
tumor-promoting
tumor-suppressor
functions
unique
complicated
implication
therapy.
also
other
signaling
networks
PI3K/Akt,
STAT3,
Wnt/β-catenin
EZH2
among
others.
Notably,
lncRNA/miRNA
considered
a
signature
for
diagnosis
prognosis
Abstract
There
are
five
fibroblast
growth
factor
receptors
(FGFRs),
namely,
FGFR1–FGFR5.
When
FGFR
binds
to
its
ligand,
(FGF),
it
dimerizes
and
autophosphorylates,
thereby
activating
several
key
downstream
pathways
that
play
an
important
role
in
normal
physiology,
such
as
the
Ras/Raf/mitogen‐activated
protein
kinase
kinase/extracellular
signal‐regulated
kinase,
phosphoinositide
3‐kinase
(PI3K)/AKT,
phospholipase
C
gamma/diacylglycerol/protein
c,
signal
transducer
activator
of
transcription
pathways.
Furthermore,
oncogene,
genetic
alterations
were
found
7.1%
tumors,
these
include
gene
amplification,
mutations,
fusions
or
rearrangements.
Therefore,
rearrangements,
considered
potential
biomarkers
therapeutic
response
for
tyrosine
inhibitors
(TKIs).
However,
is
worth
noting
with
increased
use,
resistance
TKIs
inevitably
develops,
well‐known
gatekeeper
mutations.
Thus,
overcoming
development
drug
becomes
a
serious
problem.
This
review
mainly
outlines
family
functions,
related
pathways,
agents
tumors
aim
obtaining
better
outcomes
cancer
patients
changes.
The
information
provided
this
may
provide
additional
ideas
tumor
abnormalities.
ACS Nano,
Год журнала:
2023,
Номер
17(22), С. 22240 - 22258
Опубликована: Ноя. 15, 2023
Sorafenib,
a
first-line
molecular-target
drug
for
advanced
hepatocellular
carcinoma
(HCC),
has
been
shown
to
be
potent
ferroptosis
inducer
in
HCC.
However,
we
found
that
there
was
lower
level
of
sorafenib-resistant
HCC
samples
than
sorafenib-sensitive
samples,
suggesting
sorafenib
resistance
may
result
suppression.
Recent
reports
have
long
noncoding
RNAs
(lncRNAs)
are
involved
programmed
cell
death
(PCD),
including
apoptosis
and
ferroptosis.
This
study
aimed
investigate
the
roles
underlying
molecular
mechanisms
lncRNAs
sorafenib-induced
cells.
Using
lncRNA
sequencing,
identified
ferroptosis-related
lncRNA,
URB1-antisense
RNA
1
(AS1),
which
highly
expressed
predicted
poor
survival
Furthermore,
URB1-AS1
mitigates
by
inducing
ferritin
phase
separation
reducing
cellular
free
iron
content.
Hypoxia
inducible
factor
(HIF)-1α
as
key
promoting
expression
Notably,
specifically
inhibiting
with
N-acetylgalactosamine
(GalNAc)-small
interfering
(si)URB1-AS1
successfully
enhanced
sensitivity
cells
an
vivo
tumor
model.
Our
uncovered
critical
role
repression
ferroptosis,
targeting
represent
potential
approach
overcome