Heliyon,
Год журнала:
2024,
Номер
10(10), С. e30841 - e30841
Опубликована: Май 1, 2024
Long
noncoding
RNAs
(lncRNAs)
have
emerged
as
critical
regulators
of
colorectal
cancer
(CRC)
progression,
but
their
roles
and
underlying
mechanisms
in
liver
metastases
(CRLMs)
remain
poorly
understood.
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
Abstract
Background
Colorectal
cancer
(CRC)
is
a
major
cause
of
cancer-related
deaths
worldwide,
and
chemoresistance
obstacle
in
its
treatment.
Despite
advances
therapy,
the
molecular
mechanism
underlying
CRC
not
fully
understood.
Recent
studies
have
implicated
key
roles
long
noncoding
RNAs
(lncRNAs)
regulation
chemoresistance.
Methods
In
this
study,
we
investigated
role
lncRNA
LINC01852
expression
was
evaluated
multiple
cohorts
using
quantitative
reverse
transcription
PCR.
We
conducted
vitro
vivo
functional
experiments
cell
culture
mouse
models.
RNA
pull-down,
immunoprecipitation,
chromatin
dual
luciferase
assays
were
used
to
investigate
CRC.
Results
Our
findings
revealed
that
with
tumor-inhibiting
properties,
LINC01852,
downregulated
inhibited
proliferation
both
vivo.
Further
mechanistic
investigations
increases
TRIM72-mediated
ubiquitination
degradation
SRSF5,
inhibiting
SRSF5-mediated
alternative
splicing
PKM
thereby
decreasing
production
PKM2.
Overexpression
induces
metabolic
switch
from
aerobic
glycolysis
oxidative
phosphorylation,
which
attenuates
cells
by
PKM2-mediated
glycolysis.
Conclusions
results
demonstrate
plays
an
important
repressing
malignancy
regulating
PKM,
targeting
LINC01852/TRIM72/SRSF5/PKM2
signaling
axis
may
represent
potential
therapeutic
strategy
for
Cancer Letters,
Год журнала:
2024,
Номер
598, С. 217085 - 217085
Опубликована: Июль 2, 2024
LncRNA
plays
a
crucial
role
in
cancer
progression
and
targeting,
but
it
has
been
difficult
to
identify
the
critical
lncRNAs
involved
colorectal
(CRC)
progression.
We
identified
FAM83H-AS1
as
tumor-promoting
associated
lncRNA
using
21
pairs
of
stage
IV
CRC
tissues
adjacent
normal
tissues.
In
vitro
vivo
experiments
revealed
that
knockdown
cells
inhibited
tumor
proliferation
metastasis,
vice
versa.
M6A
modification
is
for
RNA
stability
through
writer
METTL3
readers
IGF2BP2/IGFBP3.
PTBP1-an
binding
protein-is
responsible
function
CRC.
T4
(1770-2440
nt)
T5
(2440-2743
on
exon
4
provide
platform
PTBP1
RRM2
interactions.
Our
results
demonstrated
m6A
dysregulated
oncogenic
by
phosphorylated
its
splicing
effect.
patient-derived
xenograft
models,
ASO-FAM83H-AS1
significantly
suppressed
growth
gastrointestinal
(GI)
tumors,
not
only
also
GC
ESCC.
The
combination
oxaliplatin/cisplatin
compared
with
treatment
either
agent
alone.
Notably,
there
was
pathological
complete
response
all
these
three
GI
cancers.
findings
suggest
targeted
therapy
would
benefit
patients
primarily
receiving
platinum-based