Molecular Cancer,
Journal Year:
2020,
Volume and Issue:
19(1)
Published: Jan. 15, 2020
MicroRNAs
(miRNAs)
and
Twist1-induced
epithelial-mesenchymal
transition
(EMT)
in
cancer
cell
dissemination
are
well
established,
but
the
involvement
of
long
noncoding
RNAs
(lncRNAs)
Twist1-mediated
signaling
remains
largely
unknown.RT-qPCR
western
blotting
were
conducted
to
detect
expression
levels
lncRNA
JPX
Twist1
lung
lines
tissues.
The
impact
on
expression,
growth,
invasion,
apoptosis,
vivo
tumor
growth
investigated
cells
by
blotting,
rescue
experiments,
colony
formation
assay,
flow
cytometry,
xenograft
animal
experiment.We
observed
that
was
upregulated
metastatic
tissues
closely
correlated
with
size
an
advanced
stage.
Functionally,
promoted
proliferation
vitro
facilitated
vivo.
Additionally,
competitively
sponging
miR-33a-5p
subsequently
induced
EMT
invasion.
Interestingly,
coordinately
cells.
Mechanically,
JPX/miR-33a-5p/Twist1
axis
participated
progression
activating
Wnt/β-catenin
signaling.These
findings
suggest
JPX,
a
mediator
signaling,
could
predispose
metastasis
may
serve
as
potential
target
for
targeted
therapy.
International Journal of Molecular Sciences,
Journal Year:
2019,
Volume and Issue:
20(11), P. 2767 - 2767
Published: June 5, 2019
Transforming
growth
factor
β
(TGF-β)
is
a
secreted
cytokine
that
regulates
cell
proliferation,
migration,
and
the
differentiation
of
plethora
different
types.
Consistent
with
these
findings,
TGF-β
plays
key
role
in
controlling
embryogenic
development,
inflammation,
tissue
repair,
as
well
maintaining
adult
homeostasis.
elicits
broad
range
context-dependent
cellular
responses,
consequently,
alterations
signaling
have
been
implicated
many
diseases,
including
cancer.
During
early
stages
tumorigenesis,
acts
tumor
suppressor
by
inducing
cytostasis
apoptosis
normal
premalignant
cells.
However,
at
later
stages,
when
cancer
cells
acquired
oncogenic
mutations
and/or
lost
gene
function,
are
resistant
to
TGF-β-induced
arrest,
functions
promotor
stimulating
undergo
so-called
epithelial-mesenchymal
transition
(EMT).
The
latter
leads
metastasis
chemotherapy
resistance.
further
supports
progression
activating
angiogenesis
cancer-associated
fibroblasts
enabling
evade
inhibitory
immune
responses.
In
this
review,
we
will
consider
cycle
apoptosis,
EMT
metastasis.
particular,
highlight
recent
insights
into
multistep
dynamically
controlled
process
miRNAs
long
noncoding
RNAs
process.
Finally,
discuss
how
new
mechanistic
might
be
exploited
develop
novel
therapeutic
interventions.
Theranostics,
Journal Year:
2018,
Volume and Issue:
8(14), P. 3932 - 3948
Published: Jan. 1, 2018
Long
non-coding
RNAs
(lncRNAs)
are
involved
in
the
pathology
of
various
tumors,
including
colorectal
cancer
(CRC).
The
crosstalk
between
carcinoma-
associated
fibroblasts
(CAFs)
and
cells
tumor
microenvironment
promotes
development
confers
chemoresistance.
In
this
study,
we
further
investigated
underlying
tumor-promoting
roles
CAFs
molecular
mediators
these
processes.
Methods:
AOM/DSS-induced
colitis-associated
(CAC)
mouse
model
was
established,
RNA
sequencing
performed.
Small
interfering
(siRNA)
sequences
were
used
to
knock
down
H19.
Cell
apoptosis
measured
by
flow
cytometry.
SW480
with
H19
stably
knocked
establish
a
xenograft
model.
indicated
protein
levels
tissues
confirmed
immunohistochemistry
assay,
cell
analyzed
TUNEL
assay.
RNA-FISH
immunofluorescence
assays
performed
assess
expression
stroma
nests.
AldeRed
ALDH
detection
assay
detect
intracellular
aldehyde
dehydrogenase
(ALDH)
enzyme
activity.
Isolated
exosomes
identified
transmission
electron
microscopy,
nanoparticle
tracking
Western
blotting.
Results:
highly
expressed
CAC
mice
compared
normal
colon
tissues.
up-regulation
also
CRC
patient
samples
at
different
node
metastasis
(TNM)
stages.
Moreover,
stemness
stem
(CSCs)
specimens.
promoted
CSCs
increased
frequency
tumor-initiating
cells.
showed
higher
than
Of
note,
enriched
CAF-derived
conditioned
medium
exosomes,
which
turn
chemoresistance
vitro
vivo.
Furthermore,
activated
β-catenin
pathway
via
acting
as
competing
endogenous
sponge
for
miR-141
CRC,
while
significantly
inhibited
Conclusion:
promote
transferring
exosomal
miR-141,
Our
findings
indicate
that
contributes
Cell Death and Differentiation,
Journal Year:
2019,
Volume and Issue:
26(11), P. 2329 - 2343
Published: Feb. 20, 2019
The
regulatory
loop
between
long
noncoding
RNAs
(lncRNAs)
and
microRNAs
has
a
dynamic
role
in
transcriptional
translational
regulation,
is
involved
cancer.
However,
the
circuitry
lncRNAs
tumorigenesis
remains
elusive.
Here
we
demonstrate
that
nuclear
lncRNA
LINC00336
upregulated
lung
cancer
functions
as
an
oncogene
by
acting
competing
endogenous
RNA
(ceRNAs).
bound
RNA-binding
protein
ELAVL1
(ELAV-like
1)
using
nucleotides
1901–2107
of
RRM
interaction
domain
key
amino
acids
(aa)
(aa
101–213),
inhibiting
ferroptosis.
Moreover,
increased
expression
stabilizing
its
posttranscriptional
level,
whereas
LSH
(lymphoid-specific
helicase)
through
p53
signaling
pathway,
further
supporting
hypothesis
promotes
expression.
Interestingly,
served
sponge
microRNA
6852
(MIR6852)
to
regulate
cystathionine-β-synthase
(CBS),
surrogate
marker
Finally,
found
MIR6852
inhibited
cell
growth
promoting
These
data
show
network
ceRNA
important
Cancer Cell,
Journal Year:
2018,
Volume and Issue:
33(4), P. 706 - 720.e9
Published: April 1, 2018
We
characterized
the
epigenetic
landscape
of
genes
encoding
long
noncoding
RNAs
(lncRNAs)
across
6,475
tumors
and
455
cancer
cell
lines.
In
stark
contrast
to
CpG
island
hypermethylation
phenotype
in
cancer,
we
observed
a
recurrent
hypomethylation
1,006
lncRNA
including
EPIC1
(epigenetically-induced
lncRNA1).
Overexpression
is
associated
with
poor
prognosis
luminal
B
breast
patients
enhances
tumor
growth
vitro
vivo.
Mechanistically,
promotes
cell-cycle
progression
by
interacting
MYC
through
EPIC1's
129–283
nt
region.
knockdown
reduces
occupancy
its
target
(e.g.,
CDKN1A,
CCNA2,
CDC20,
CDC45).
depletion
abolishes
regulation
tumorigenesis