Molecular Cancer,
Journal Year:
2020,
Volume and Issue:
19(1)
Published: Aug. 7, 2020
N6-methyladenosine
(m6A)
is
one
of
the
most
common
RNA
modifications
in
eukaryotes,
mainly
messenger
(mRNA).
Increasing
evidence
shows
that
m6A
methylation
modification
acts
an
essential
role
various
physiological
and
pathological
bioprocesses.
Noncoding
RNAs
(ncRNAs),
including
miRNAs,
lncRNAs
circRNAs,
are
known
to
participate
regulating
cell
differentiation,
angiogenesis,
immune
response,
inflammatory
response
carcinogenesis.
regulators,
such
as
METTL3,
ALKBH5
IGF2BP1
have
been
reported
execute
a
m6A-dependent
ncRNAs
involved
Meanwhile,
can
target
or
modulate
regulators
influence
cancer
development.
In
this
review,
we
provide
insight
into
interplay
between
cancer.
Journal of Cellular Physiology,
Journal Year:
2020,
Volume and Issue:
236(4), P. 2649 - 2658
Published: Sept. 6, 2020
Abstract
N
6
‐methyladenosine
(m
A)
and
long
noncoding
RNAs
(lncRNAs)
are
both
crucial
regulators
in
non‐small‐cell
lung
cancer
(NSCLC)
tumorigenesis.
However,
the
pathological
roles
of
m
A
lncRNAs
NSCLC
progression
still
limited
undefined.
Here,
lncRNA
ABHD11‐AS1
was
upregulated
tissue
specimens
cells
ectopic
overexpression
closely
correlated
with
unfavorable
prognosis
patients.
Functionally,
promoted
proliferation
Warburg
effect
NSCLC.
Mechanistically,
profile
analyzed
by
methylated
RNA
immunoprecipitation
sequencing
(MeRIP‐Seq).
MeRIP‐Seq
presented
that
there
modification
site
ABHD11‐AS1.
methyltransferase‐like
3
(METTL3)
installed
enhanced
transcript
stability
to
increase
its
expression.
In
conclusion,
our
findings
highlight
function
mechanism
METTL3‐induced
inspire
understanding
biology.
Clinical and Translational Medicine,
Journal Year:
2021,
Volume and Issue:
11(6)
Published: June 1, 2021
Abstract
Background
Bone
metastasis
is
the
leading
cause
of
tumor‐related
death
in
prostate
cancer
(PCa)
patients.
Long
noncoding
RNAs
(lncRNAs)
have
been
well
documented
to
be
involved
progression
multiple
cancers.
Nevertheless,
role
lncRNAs
PCa
bone
remains
largely
unclear.
Methods
The
expression
cancer‐associated
transcripts
was
analyzed
published
datasets
and
further
verified
clinical
samples
cell
lines
by
RT‐qPCR
situ
hybridization
assays.
Colony
formation
assay,
MTT
cycle
analysis,
EdU
Transwell
migration
invasion
assays,
wound
healing
vivo
experiments
were
carried
out
investigate
function
transcript
6
(
PCAT6
)
tumor
growth
PCa.
Bioinformatic
RNA
pull‐down,
RIP
assays
conducted
identify
proteins
binding
potential
targets
.
therapeutic
targeting
antisense
oligonucleotides
(ASO)
explored
Results
upregulated
tissues
with
increased
predicted
poor
prognosis
Functional
found
that
knockdown
significantly
inhibited
invasion,
migration,
proliferation
vitro
,
as
Mechanistically,
METTL3
‐mediated
m
A
modification
contributed
upregulation
an
IGF2BP2
‐dependent
manner.
Furthermore,
IGF1R
enhancing
mRNA
stability
through
/
RNA‐protein
three‐dimensional
complex.
Importantly,
inhibition
ASO
showed
against
Finally,
correlation
demonstrated
cells.
Conclusions
Our
study
uncovers
a
novel
molecular
mechanism
which
A‐induced
axis
promotes
growth,
suggesting
may
serve
promising
prognostic
marker
target
bone‐metastatic
Biomedicine & Pharmacotherapy,
Journal Year:
2021,
Volume and Issue:
143, P. 112132 - 112132
Published: Sept. 1, 2021
Fibrosis
is
the
endpoint
of
pathological
remodeling.
This
process
contributes
to
pathogenesis
several
chronic
disorders
and
aging-associated
organ
damage.
Different
molecular
cascades
contribute
this
process.
TGF-β,
WNT,
YAP/TAZ
signaling
pathways
have
prominent
roles
in
A
number
long
non-coding
RNAs
microRNAs
been
found
regulate
fibrosis
through
modulation
activity
related
pathways.
miR-144-3p,
miR-451,
miR-200b,
miR-328
are
among
that
participate
pathology
cardiac
fibrosis.
Meanwhile,
miR-34a,
miR-17-5p,
miR-122,
miR-146a,
miR-350
liver
different
situations.
PVT1,
MALAT1,
GAS5,
NRON,
PFL,
MIAT,
HULC,
ANRIL,
H19
We
review
impact
aging-related
pathologies.
Journal of Cellular and Molecular Medicine,
Journal Year:
2021,
Volume and Issue:
25(16), P. 7660 - 7674
Published: June 24, 2021
Abstract
Renal
fibrosis
induced
by
urinary
tract
obstruction
is
a
common
clinical
occurrence;
however,
effective
treatment
lacking,
and
deeper
understanding
of
the
mechanism
renal
needed.
Previous
studies
have
revealed
that
miR‐21
impacts
liver
lung
progression
activating
SPRY1/ERK/NF‐kB
signalling
pathway.
However,
whether
mediates
obstructive
through
same
pathway
has
not
been
determined.
Additionally,
shown
N6‐methyladenosine
(m
6
A)
modification‐dependent
primary
microRNA
(pri‐microRNA)
processing
essential
for
maturation
microRNAs,
but
its
role
in
yet
investigated
detail.
To
address
these
issues,
we
employed
mouse
model
unilateral
ureteral
(UUO)
which
left
ureters
were
ligated
3,
7
14
days
to
simulate
fibrotic
process.
In
vitro,
human
proximal
tubular
epithelial
(HK‐2)
cells
transfected
with
plasmids
containing
corresponding
sequence
METTL3,
miR‐21‐5p
mimic
or
inhibitor.
We
found
levels
m
A
modification
UUO
groups
increased
significantly,
as
predicted,
was
activated
miR‐21‐5p,
confirming
plays
an
important
enhancing
inflammation.
METTL3
play
major
catalytic
mice
drove
development
promoting
maturation.
Our
research
first
demonstrate
METTL3‐m
A‐miR‐21‐5p‐SPRY1/ERK/NF‐kB
axis
provides
fibrosis.
Journal of Hematology & Oncology,
Journal Year:
2022,
Volume and Issue:
15(1)
Published: July 6, 2022
Abstract
The
tumor
microenvironment
(TME),
which
is
regulated
by
intrinsic
oncogenic
mechanisms
and
epigenetic
modifications,
has
become
a
research
hotspot
in
recent
years.
Characteristic
features
of
TME
include
hypoxia,
metabolic
dysregulation,
immunosuppression.
One
the
most
common
RNA
N6-methyladenosine
(m
6
A)
methylation,
widely
involved
regulation
physiological
pathological
processes,
including
development.
Compelling
evidence
indicates
that
m
A
methylation
regulates
transcription
protein
expression
through
shearing,
export,
translation,
processing,
thereby
participating
dynamic
evolution
TME.
Specifically,
methylation-mediated
adaptation
to
phenotypic
shift
immune
cells
synergistically
promote
formation
an
immunosuppressive
supports
proliferation
metastasis.
In
this
review,
we
have
focused
on
involvement
tumor-adaptive
described
detailed
linking
change
cell
biological
functions.
view
collective
data,
advocate
treating
as
complete
ecosystem
components
crosstalk
with
each
other
achieve
adaptive
changes.
Finally,
describe
potential
utility
methylation-targeted
therapies
immunotherapy
clinical
applications
challenges
faced,
aim
advancing
research.
Cell Death and Disease,
Journal Year:
2023,
Volume and Issue:
14(2)
Published: Feb. 15, 2023
Dysfunction
of
podocytes
has
been
regarded
as
an
important
early
pathologic
characteristic
diabetic
kidney
disease
(DKD),
but
the
regulatory
role
long
noncoding
RNAs
(lncRNAs)
in
this
process
remains
largely
unknown.
Here,
we
performed
RNA
sequencing
tissues
isolated
from
DKD
patients
and
nondiabetic
renal
cancer
undergoing
surgical
resection
discovered
that
novel
lncRNA
ENST00000436340
was
upregulated
high
glucose-induced
podocytes,
showed
a
significant
correlation
between
injury.
Gain-
loss-of-function
experiments
silencing
alleviated
podocyte
injury
cytoskeleton
rearrangement.
Mechanistically,
fat
mass
obesity-
associate
gene
(FTO)-mediated
m6A
induced
upregulation
ENST00000436340.
interacted
with
polypyrimidine
tract
binding
protein
1
(PTBP1)
augmented
PTBP1
to
RAB3B
mRNA,
promoted
mRNA
degradation,
thereby
caused
rearrangement
inhibition
GLUT4
translocation
plasma
membrane,
leading
progression.
Together,
our
results
suggested
could
promote
through
PTBP1-dependent
regulation,
thus
suggesting
form
lncRNA-mediated
epigenetic
regulation
contributes
pathogenesis
DKD.
