annals of urologic oncology,
Journal Year:
2023,
Volume and Issue:
unknown
Published: Nov. 11, 2023
Prostate
cancer
(Pca)
remains
the
most
common
malignancy
worldwide
in
men,
and
second
leading
cause
of
mortality
only
to
lung
cancer.
Besides
surgery,
androgen
deprivation
therapy
(ADT)
is
a
major
treatment
for
Pca.
However,
ADT
leads
inevitable
progression
castration-resistant
Pca
(CRPC).
The
transition
from
hormone-dependent
(ADPC)
CRPC
has
been
shown
involve
reactivation
receptor
(AR)
signaling
pathway.
evidence
become
strong
that
develop
adaptive
mechanisms
maintaining
AR
allow
survival
further
evolution.
This
article
mainly
reviews
research
progress
mechanism(s)
provides
scientific
basis
new
ideas
diagnosis
this
phenotype.
Molecular Cancer,
Journal Year:
2024,
Volume and Issue:
23(1)
Published: Aug. 30, 2024
Drug
resistance
in
cancer
cells
significantly
diminishes
treatment
efficacy,
leading
to
recurrence
and
metastasis.
A
critical
factor
contributing
this
is
the
epigenetic
alteration
of
gene
expression
via
RNA
modifications,
such
as
N6-methyladenosine
(m6A),
N1-methyladenosine
(m1A),
5-methylcytosine
(m5C),
7-methylguanosine
(m7G),
pseudouridine
(Ψ),
adenosine-to-inosine
(A-to-I)
editing.
These
modifications
are
pivotal
regulating
splicing,
translation,
transport,
degradation,
stability.
Governed
by
"writers,"
"readers,"
"erasers,"
impact
numerous
biological
processes
progression,
including
cell
proliferation,
stemness,
autophagy,
invasion,
apoptosis.
Aberrant
can
lead
drug
adverse
outcomes
various
cancers.
Thus,
targeting
modification
regulators
offers
a
promising
strategy
for
overcoming
enhancing
efficacy.
This
review
consolidates
recent
research
on
role
prevalent
resistance,
with
focus
m6A,
m1A,
m5C,
m7G,
Ψ,
A-to-I
Additionally,
it
examines
regulatory
mechanisms
linked
underscores
existing
limitations
field.
Small,
Journal Year:
2024,
Volume and Issue:
20(30)
Published: Feb. 29, 2024
Abstract
Tumor‐derived
exosomes
(TDEs)
induced
extracellular
microenvironment
has
recently
been
validated
to
be
critical
for
tumor
progression
and
metastasis,
however,
remodeling
it
oncotherapy
still
remains
a
major
challenge
due
difficulty
in
regulation
of
TDEs
secretion.
Herein,
the
supramolecular
chiral
nanofibers,
composed
L/D
‐phenylalanine
derivates
(L/D‐Phe)
linear
hyaluronic
acid
(HA),
are
successfully
employed
construct
anti‐tumor
microenvironment.
The
left‐handed
L‐Phe
@HA
nanofibers
significantly
inhibit
secretion
into
microenvironment,
which
results
suppression
proliferation
metastasis
vitro
vivo.
Biological
assays
theoretical
modeling
reveal
that
these
mainly
attributed
strong
adsorption
key
transporters
(Ras‐related
protein
Rab‐27A
synaptosome‐associated
23)
on
via
enhanced
stereoselective
interaction,
leading
degradation
phosphorylated
dropping
transporters.
Subsequently,
transfer
function
is
limited,
causes
remarkable
inhibition
These
findings
provide
promising
novel
insight
functional
materials
establish
an
Cell Death and Disease,
Journal Year:
2024,
Volume and Issue:
15(4)
Published: April 17, 2024
Abstract
N6-methyladenosine
(m6A)
methylation,
a
prevalent
eukaryotic
post-transcriptional
modification,
is
involved
in
multiple
biological
functions,
including
mediating
variable
splicing,
RNA
maturation,
transcription,
and
nuclear
export,
also
vital
for
regulating
translation,
stability,
cytoplasmic
degradation.
For
example,
m6A
methylation
can
regulate
pre-miRNA
expression
by
affecting
both
splicing
maturation.
Non-coding
(ncRNA),
which
includes
microRNAs
(miRNAs),
long
non-coding
RNAs
(lncRNAs),
circular
(circRNAs),
does
not
encode
proteins
but
has
powerful
impacts
on
transcription
translation.
Conversely,
ncRNAs
may
impact
the
of
regulators,
miRNAs
targeting
mRNA
or
lncRNAs,
circRNAs,
acting
as
scaffolds
to
regulatory
factors.
Dysregulation
common
urinary
tumors,
role
important
these
malignancies.
This
article
provides
systematic
review
mechanisms
action
tumors.
Cell Death and Disease,
Journal Year:
2025,
Volume and Issue:
16(1)
Published: April 12, 2025
Fibroblast-to-myofibroblast
differentiation
is
the
main
cytopathologic
characteristic
of
pulmonary
fibrosis.
However,
its
underlying
molecular
mechanism
remains
poorly
understood.
This
study
elucidated
that
nuclear
export
lncNONMMUT062668.2
(lnc668)
exacerbated
fibrosis
by
activating
fibroblast-to-myofibroblast
differentiation.
Mechanistic
research
revealed
histone
H3K9
lactylation
in
promoter
region
N6-methyladenosine
(m6A)
writer
METTL3
was
enriched
to
enhance
transcription,
leading
lnc668
m6A
modification.
Meanwhile,
reader
YTHDC1
recognized
m6A-modified
and
elevated
METTL3-mediated
Subsequently,
phase-separating
promoted
lnc668.
In
this
process,
formed
a
pore
complex
with
serine/arginine-rich
splicing
factor
3,
Aly/REF
factor,
exportin-5
assist
translocation
from
nucleus
cytoplasm.
After
export,
facilitated
translation
stability
host
gene
phosphatidylinositol-binding
clathrin
assembly
protein
activate
differentiation,
aggravation
fibrosis,
which
also
depended
on
phase
separation.
first
clarified
separation
crucial
for
modification,
profibrotic
role
exacerbating
These
findings
provide
new
insights
into
cytoplasmic
lncRNAs
identified
potential
targets
therapy.
Clinical and Experimental Medicine,
Journal Year:
2025,
Volume and Issue:
25(1)
Published: May 3, 2025
Lung
squamous
cell
carcinoma
(LUSC),
a
major
subtype
of
non-small
lung
cancer,
remains
challenging
to
treat
due
poor
prognosis
and
limited
therapeutic
options.
This
study
investigates
the
prognostic
implications
copper-induced
death-related
long
non-coding
RNAs
(lncRNAs)
in
LUSC
using
data
from
The
Cancer
Genome
Atlas.
Five
lncRNAs
(AC010328.1,
LINC01740,
AL358613.2,
MIR3945HG,
AC002467.1)
were
identified
as
independent
markers
incorporated
into
risk
score
model
stratify
patients
high-
low-risk
groups.
Survival
analyses
revealed
significant
differences
overall
survival,
with
high-risk
group
exhibiting
higher
immune
evasion
potential
poorer
response
immunotherapy.
Functional
enrichment
highlighted
involvement
these
drug
metabolism
tumor
biology.
Furthermore,
mutation
burden
analysis
dysfunction
evaluation
confirmed
clinical
relevance
model,
identifying
more
sensitive
targeted
drugs
such
Quizartinib
Dasatinib.
A
Nomogram
integrating
lncRNA
scores
factors
demonstrated
robust
predictive
accuracy
for
1-,
3-,
5-year
survival
outcomes.
provides
novel
biomarkers
actionable
insights
improving
assessment
personalizing
immunotherapy
strategies
patients.
Journal of Cellular and Molecular Medicine,
Journal Year:
2024,
Volume and Issue:
28(10)
Published: May 1, 2024
Hepatocellular
carcinoma
(HCC)
presents
a
persistent
challenge
to
conventional
therapeutic
approaches.
SLC12A5
is
implicated
in
an
oncogenic
capacity
and
facilitates
the
progression
of
cancer.
The
objective
this
investigation
scrutinize
inhibitory
effects
borax
on
endoplasmic
reticulum
(ER)-stress
apoptosis
mediated
by
HepG2
cells.
Initially,
we
evaluated
cytotoxic
impact
both
HL-7702
cell
lines.
Subsequently,
cellular
morphology
cycle
these
lines
were
examined.
Following
this,
explored
treatment
mRNA
protein
expression
levels
SLC12A5,
C/EBP
homologous
(CHOP),
glucose-regulated
protein-78
(GRP78),
activating
transcription
factor-6
(ATF6),
caspase-3
(CASP3),
cytochrome
c
(CYC)
populations.
determined
IC50
value
for
cells
was
40.8
mM,
whereas
cells,
22.6
mM.
concentrations
(22.6
mM)
IC75
(45.7
did
not
manifest
morphological
aberrations
Conversely,
induced
observable
nuclear
abnormalities,
resulting
arrest
G1/G0
phase.
Additionally,
ATF6,
CHOP,
GRP78,
CASP3,
CYC
elevated
comparison
Moreover,
decreased
following
exhibited
significant
increase.
In
conclusion,
our
data
highlight
potential
through
regulation
ER
stress
HCC
targeting
SLC12A5.