LncRNA01103/FGF13 axis promotes the progression of bone cancer pain by remodeling ac4C modification
Abstract
Bone
cancer
pain
(BCP)
significantly
impacts
patients'
quality
of
life,
yet
its
causes
and
mechanisms
remain
unclear.
Long
noncoding
RNAs
(lncRNAs)
have
gained
attention
for
their
regulatory
role
in
disease
processes.
Through
analysis
validating
acRIP-seq
data
from
our
previous
study,
we
discovered
that
lncRNA01103
undergoes
N4-acetylcytidine
(ac4C)
modification
increased
expression
the
SDH
BCP
rats.
Interestingly,
ac4C
influences
stability
lncRNA01103,
impacting
levels.
Further
experiments
revealed
is
localized
neurons
translocated
towards
nucleus
Knockdown
reversed
BCP,
spinal
c-fos
neuron
sensitization,
pain-related
negative
behaviors.
Transcriptomic
identified
FGF13
as
a
key
target
neuronal
nucleus,
with
inhibition
alleviating
downregulating
Nav1.7
sodium
channel
Validation
lncRNA01103's
regulating
behaviors
was
confirmed
through
lncRNA01103-ASO
sequence.
This
study
highlights
NAT10/ac4C-mediated
posttranscriptional
modulation
activating
FGF13-Nav1.7
signaling
pathway
inducing
hypersensitivity
Targeting
could
provide
novel
therapeutic
strategy
BCP.
Research Square (Research Square), Год журнала: 2024, Номер unknown
Опубликована: Сен. 3, 2024
Язык: Английский