Research Square (Research Square),
Год журнала:
2023,
Номер
unknown
Опубликована: Сен. 18, 2023
Abstract
C
18
H
17
NO
6
(Aucan)
is
derived
from
a
special
plant
in
Yunnan
Province,
Lichen
Lethariella
cladonioides,
which
also
traditional
medicine
Province.
A
novel
natural
anticancer
active
molecule
obtained
chloroform
extract
of
leaf
moth
(Lethariella
cladonioides)
by
utilizing
photochemical
techniques
(patent
No.
201710388136.8).
Has
certain
curative
effect
on
glioma.
Choosing
Aucan
treated
human
U251
and
LN229
glioma
cell
lines,
CCK-8
assay
was
used
to
detect
IC50
Aucan,
MTT
assay,
Colony
formation
Flow
cytometry,
Wound
healing
Transwell
experiment
were
evaluate
the
effects
proliferation,
migration
apoptosis
cells.
The
studied
constructing
subcutaneous
tumor
model
nude
mice
obtaining
relevant
data
such
as
image,
volume
survival
time.
molecular
target
affecting
searched
through
network
pharmacology,
EGLN1
found
be
key
gene.
can
affect
proliferation
cells,
inhibit
growth
improve
rate
mice.
Bioinformatics
analysis
that
associated
with
autophagy
apoptosis.
qPCR
detected
significant
expression
tissue
cells
decreased
after
treatment.
experimental
results
showed
did
occurrence
autophagy,
induced
autophagy.
this
study
indicate
via
regulating
EGLN1,
thus
development
tumors.
Pharmacological Research,
Год журнала:
2022,
Номер
187, С. 106553 - 106553
Опубликована: Ноя. 16, 2022
Cancer
progression
results
from
activation
of
various
signaling
networks.
Among
these,
PI3K/Akt
contributes
to
proliferation,
invasion,
and
inhibition
apoptosis.
Hepatocellular
carcinoma
(HCC)
is
a
primary
liver
cancer
with
high
incidence
rate,
especially
in
regions
prevalence
viral
hepatitis
infection.
Autoimmune
disorders,
diabetes
mellitus,
obesity,
alcohol
consumption,
inflammation
can
also
lead
initiation
development
HCC.
The
treatment
HCC
depends
on
the
identification
oncogenic
factors
that
tumor
cells
develop
resistance
therapy.
present
review
article
focuses
role
progression.
Activation
promotes
glucose
uptake,
favors
glycolysis
increases
cell
proliferation.
It
inhibits
both
apoptosis
autophagy
while
promoting
survival.
stimulates
epithelial-to-mesenchymal
transition
(EMT)
matrix-metalloproteinase
(MMP)
expression
during
metastasis.
In
addition
increasing
colony
formation
capacity
facilitating
spread
cells,
angiogenesis.
Therefore,
silencing
prevents
aggressive
behavior.
confer
drug
resistance,
particularly
sorafenib,
decreases
radio-sensitivity
cells.
Anti-cancer
agents,
like
phytochemicals
small
molecules
suppress
by
limiting
Being
upregulated
tissues
clinical
samples,
be
used
as
biomarker
predict
patients'
response
Biomedicine & Pharmacotherapy,
Год журнала:
2022,
Номер
154, С. 113609 - 113609
Опубликована: Авг. 27, 2022
Epigenetic
factors
are
critical
regulators
of
biological
and
pathological
mechanisms
they
could
interact
with
different
molecular
pathways.
Targeting
epigenetic
has
been
an
idea
approach
in
disease
therapy,
especially
cancer.
Accumulating
evidence
highlighted
function
long
non-coding
RNAs
(lncRNAs)
as
cancer
initiation
development
focused
on
their
association
downstream
targets.
microRNAs
(miRNAs)
the
most
well-known
targets
lncRNAs
present
review
focuses
lncRNA-miRNA
axis
malignancy
therapy
resistance
tumors.
LncRNA-miRNA
regulates
cell
death
such
apoptosis
autophagy
cancers.
This
affects
tumor
metastasis
via
regulating
EMT
MMPs.
Besides,
determines
sensitivity
cells
to
chemotherapy,
radiotherapy
immunotherapy.
Based
studies,
can
be
affected
by
drugs
genetic
tools
this
may
affect
expression
level
miRNAs
targets,
leading
suppression/progression.
LncRNAs
have
both
tumor-promoting
tumor-suppressor
functions
unique
complicated
implication
therapy.
also
other
signaling
networks
PI3K/Akt,
STAT3,
Wnt/β-catenin
EZH2
among
others.
Notably,
lncRNA/miRNA
considered
a
signature
for
diagnosis
prognosis
Frontiers in Cell and Developmental Biology,
Год журнала:
2023,
Номер
11
Опубликована: Май 5, 2023
Long
non-coding
RNAs
(lncRNAs)
play
vital
roles
in
regulating
epigenetic
mechanisms
and
gene
expression
levels,
their
dysregulation
is
closely
associated
with
a
variety
of
diseases
such
as
cancer.
Several
studies
have
demonstrated
that
lncRNAs
are
dysregulated
during
tumor
progression.
Recently,
the
MYC-induced
long
RNA
MINCR,
newly
identified
lncRNA,
has
been
to
act
an
oncogene
different
cancers,
including
gallbladder
cancer,
hepatocellular
colorectal
non-small
cell
lung
oral
squamous
carcinoma,
nasopharyngeal
glioma.
Moreover,
MINCR
reported
biomarker
prognosis
patients
cancers.
In
this
review,
we
summarize
analyze
oncogenic
human
cancers
terms
its
clinical
significance,
biological
functions,
cellular
activities,
regulatory
mechanism.
Our
analysis
literature
suggests
potential
novel
therapeutic
target
Objective:
Gliomas
as
primary
cerebral
malignancies
frequently
occurring
in
adults
have
relatively
high
morbidity
and
mortality.
The
underlying
role
of
long
non-coding
ribonucleic
acids
(lncRNAs)
has
attracted
much
attention,
among
which
tumor
suppressor
candidate
7
(TUSC7)
is
a
novel
gene
whose
regulatory
mechanism
human
gliomas
remains
inconclusive.
Methods
results:
In
this
study,
bioinformatics
analysis
indicated
that
TUSC7
could
specifically
bind
to
microRNA
(miR)-10a-5p,
according
quantitative
polymerase
chain
reaction
(q-PCR),
miR-10a-5p
was
up-regulated
glioma
cells
negatively
correlated
with
expression.
Dual-luciferase
reporter
assay
showed
the
ability
miR-10a-5p,
overexpression
notably
inhibited
expression,
restrained
cell
proliferation
migration,
regulated
cycle
cyclin
expression
via
brain-derived
neurotrophic
factor/extracellular
signal-regulated
kinase
(BDNF/ERK)
pathway.
inhibitory
effect
on
also
verified
by
designing
knockdown
panels
for
wound
healing,
Transwell
Western
blotting
assays.
Conclusions:
suppresses
migration
modulating
inhibiting
BDNF/ERK
pathway,
thus
acting
gliomas.
Frontiers in Immunology,
Год журнала:
2022,
Номер
13
Опубликована: Июнь 14, 2022
Background
Glioma,
the
most
frequent
malignant
tumor
of
neurological
system,
has
a
poor
prognosis
and
treatment
problems.
Glioma’s
microenvironment
is
also
little
known.
Methods
We
downloaded
glioma
data
from
TCGA
database.
The
patients
in
database
were
split
into
two
groups,
one
for
training
other
validation.
ubiquitination
genes
then
evaluated
using
COX
Lasso
regression
to
create
ubiquitination-related
signature.
assessed
signature’s
predictive
usefulness
role
immune
after
it
was
generated.
Finally,
vitro
experiment
utilized
check
expression
function
key
gene,
USP4.
Results
This
signature
can
be
used
categorize
patients.
Glioma
separated
high-risk
low-risk
groups
both
validation
cohorts,
with
group
having
significantly
worse
(P<0.05).
Following
further
investigation
microenvironment,
discovered
that
this
risk
grouping
could
serve
as
guide
immunotherapy.
activity,
invasion
migration
capacity,
colony
formation
ability
U87-MG
LN229
cell
lines
drastically
reduced
important
gene
USP4
knocked
down
tests.
Overexpression
A172
line,
on
hand,
greatly
improved
clonogenesis,
migration.
Conclusions
Our
research
established
foundation
understanding
gliomas
identified
possible
biomarker.
Evidence-based Complementary and Alternative Medicine,
Год журнала:
2022,
Номер
2022, С. 1 - 8
Опубликована: Июль 9, 2022
Angelica
sinensis
polysaccharide
(ASP)
is
a
traditional
herbal
medicine
accompanied
by
antitumor
potential.
This
study
aims
to
explore
the
therapeutic
potential
of
ASP
on
glioma,
as
well
underlying
mechanisms
involving
microRNA-373-3p
(miR-373-3p)
and
TGF-β/Smad4
signaling
pathway.U251
cells
(a
human
glioma
cell
line)
were
treated
with
different
concentrations
ASP.
miR-373-3p
was
silenced
in
U251
transfection
inhibitor.
Cell
viability
apoptosis
measured
CCK-8
assay
flow
cytometry,
respectively.
migration
invasion
detected
wound
healing
transwell
assays,
The
expression
RT-qPCR.
protein
expressions
TGF-β
Smad4
evaluated
both
western
blotting
immunofluorescence.ASP
inhibited
viability,
migration,
invasion,
enhanced
dose-dependent
manner.
increased
decreased
cells.
Silencing
weakened
effects
inhibiting
promoting
apoptosis.
In
addition,
deleting
pathway
cells.ASP
suppresses
malignant
progression
via
regulating
miR-373-3p-mediated
pathway.
Translational Cancer Research,
Год журнала:
2022,
Номер
11(11), С. 4126 - 4136
Опубликована: Ноя. 1, 2022
Connexin
(CX)
43
makes
glioblastoma
resistant
to
temozolomide,
the
first-line
chemotherapy
drug.
However,
targeting
CX43
is
very
difficult
because
mechanisms
underlying
CX43-mediated
resistance
remain
unclear.
highly
expressed
in
glioblastoma,
which
closely
associated
with
poor
prognosis
and
resistance.
The
present
study
was
analyze
mechanism
of
microRNA
(miR)-1
regulating
proliferation
invasion
glioma
cells.The
effects
knockdown
miR-1
on
growth
cell
lines
were
observed
by
establishing
blank,
inhibitor,
mimic
groups.
Cell
detected
using
a
Counting
Kit-8
(CCK-8)
assay,
apoptosis
flow
cytometry,
protein
expression
western
blot.
We
used
Student's
t-test
assess
continuous
data
between
two
groups
Kruskal-Wallis
test
adopted
for
multiple
group
comparisons.Compared
mimics
normal
control
(NC)
group,
rate
miR-1-3p
decreased,
while
that
inhibitor
increased
compared
NC
group.
In
addition,
model
U251
cells
exerted
an
inhibitory
effect
ability
cells,
whereas
showed
invasion-promoting
effect.
dual-luciferase
assay
had
targeted
relationship
gene.Down-regulation
inhibited
infiltration
further
promoted
expression.