Pharmacological Research,
Год журнала:
2022,
Номер
187, С. 106582 - 106582
Опубликована: Ноя. 25, 2022
Cancer
is
the
manifestation
of
changes
and
mutations
in
genetic
epigenetic
levels.
Non-coding
RNAs
(ncRNAs)
are
commonly
dysregulated
disease
pathogenesis,
their
role
cancer
has
been
well-documented.
The
ncRNAs
regulate
various
molecular
pathways
mechanisms
that
can
lead
to
induction/inhibition
carcinogenesis.
Autophagy
a
"self-digestion"
mechanism
its
function
be
pro-survival
or
pro-death
tumor
cells.
aim
present
review
evaluate
regulating
autophagy
gastrointestinal
tumors.
ncRNA/autophagy
axis
affecting
progression
gastric,
liver,
colorectal,
pancreatic,
esophageal,
gallbladder
cancers
investigated.
Both
as
oncogenic
onco-suppressor
this
interaction
determine
growth,
invasion,
therapy
response
reduce/increase
proliferation
tumors
via
glycolysis
mechanism.
Furthermore,
related
metastasis,
such
EMT
MMPs,
affected
by
axis.
chemotherapy
radiotherapy
suppressed
autophagy,
essential
regulators
miRNAs
genes
proteins
ATGs
Beclin-1.
lncRNAs
circRNAs
down-regulate
miRNA
expression
sponging
modulate
Moreover,
anti-cancer
agents
affect
level
Therefore,
translating
these
findings
into
clinics
improve
prognosis
patients.
Biomedicine & Pharmacotherapy,
Год журнала:
2023,
Номер
158, С. 114204 - 114204
Опубликована: Янв. 4, 2023
Glioblastoma
(GBM)
is
one
of
the
most
malignant
cancers
central
nervous
system
and
due
to
its
sensitive
location,
surgical
resection
has
high
risk
therefore,
chemotherapy
radiotherapy
are
utilized
for
treatment.
However,
chemoresistance
radio-resistance
other
problems
in
GBM
Hence,
new
therapies
based
on
genes
recommended
treatment
GBM.
PTEN
a
tumor-suppressor
operator
cancer
that
inhibits
PI3K/Akt/mTOR
axis
diminishing
growth,
metastasis
drug
resistance.
In
current
review,
function
PTEN/PI3K/Akt
progression
evaluated.
Mutation
or
depletion
leads
increase
progression.
Low
expression
level
mediates
poor
prognosis
by
increasing
proliferation
invasion,
promotes
malignancy
tumor
cells.
Moreover,
loss
signaling
can
result
therapy
resistance
Activation
impairs
metabolism
via
glycolysis
inhibition.
contrast
PTEN,
PI3K/Akt
oncogenic
during
progression,
enhances.
shows
positive
association
with
pathways
similar
signaling,
regulated
non-coding
RNAs.
upregulation
inhibition
anti-cancer
agents
be
beneficial
interfering
This
review
emphasizes
networks
related
provides
insights
targeting
this
effective
Pharmacological Research,
Год журнала:
2023,
Номер
194, С. 106822 - 106822
Опубликована: Июнь 17, 2023
Pancreatic
cancer
(PC)
is
a
serious
gastrointestinal
tract
disease
for
which
the
5-year
survival
rate
less
than
10%,
even
in
developed
countries
such
as
USA.
The
genomic
profile
alterations
and
dysregulated
biological
mechanisms
commonly
occur
PC.
Macroautophagy/autophagy
cell
death
process
that
maintained
at
basal
level
physiological
conditions,
whereas
its
often
changes
during
tumorigenesis.
function
of
autophagy
human
cancers
dual
can
be
oncogenic
onco-suppressor.
Autophagy
potent
controller
tumorigenesis
supportive
PC
escalates
growth
cells
suppression
mediate
death.
also
determines
metastasis
cells,
it
control
EMT
affecting
migration.
Moreover,
starvation
hypoxia
stimulate
glycolysis,
glycolysis
induction
mediated
by
enhancing
Furthermore,
protective
stimulates
drug
resistance
gemcitabine
inhibition
enhance
radiosensitivity.
degrade
MHC-I
to
immune
evasion
regulates
polarization
macrophages
tumor
microenvironment.
Modulation
activity
provided
silibinin,
ursolic
acid,
chrysin
huaier
treatment
Non-coding
RNAs
are
controllers
improve
therapy
response
patients.
mitophagy
shows
dysregulation
PC,
proliferation
cells.
Therefore,
bioinformatics
analysis
demonstrates
autophagy-related
proteins
genes
biomarkers.
Medicinal Research Reviews,
Год журнала:
2023,
Номер
43(5), С. 1263 - 1321
Опубликована: Март 23, 2023
Abstract
Gastrointestinal
(GI)
tumors
(cancers
of
the
esophagus,
gastric,
liver,
pancreas,
colon,
and
rectum)
contribute
to
a
large
number
deaths
worldwide.
STAT3
is
an
oncogenic
transcription
factor
that
promotes
genes
associated
with
proliferation,
antiapoptosis,
survival,
metastasis.
overactivated
in
many
human
malignancies
including
GI
which
accelerates
tumor
progression,
metastasis,
drug
resistance.
Research
recent
years
demonstrated
noncoding
RNAs
(ncRNAs)
play
major
role
regulation
signaling
pathways
pathway.
The
types
endogenous
ncRNAs
are
being
extensively
studied
oncology
microRNAs,
long
RNAs,
circular
RNAs.
These
can
either
be
tumor‐promoters
or
tumor‐suppressors
each
one
them
imparts
their
activity
via
different
mechanisms.
pathway
also
tightly
modulated
by
ncRNAs.
In
this
article,
we
have
elaborated
on
tumor‐promoting
tumors.
Subsequently,
comprehensively
discussed
as
well
suppressor
functions
mechanism
action
known
modulate
cancers.
Cancer Gene Therapy,
Год журнала:
2024,
Номер
31(6), С. 816 - 830
Опубликована: Фев. 14, 2024
Abstract
RNA
modification,
especially
N6-methyladenosine,
5-methylcytosine,
and
N7-methylguanosine
methylation,
participates
in
the
occurrence
progression
of
cancer
through
multiple
pathways.
The
function
expression
these
epigenetic
regulators
have
gradually
become
a
hot
topic
research.
Mutation
regulation
noncoding
RNA,
lncRNA,
play
major
role
cancer.
Generally,
lncRNAs
exert
tumor-suppressive
or
oncogenic
functions
its
dysregulation
can
promote
tumor
metastasis.
In
this
review,
we
summarize
modifications
lncRNAs.
Furthermore,
discuss
relationship
between
modification
lncRNA
interaction
various
cancers.
Therefore,
review
gives
comprehensive
understanding
mechanisms
by
which
affects
cancers
regulating
lncRNAs,
may
shed
new
light
on
research
provide
insights
into
therapy.
Breast Cancer,
Год журнала:
2024,
Номер
31(4), С. 607 - 620
Опубликована: Июнь 4, 2024
Abstract
Objective
Breast
cancer
is
one
of
the
most
prevalent
malignancies
in
women.
Exosomes
are
important
mediators
intercellular
communication;
however,
their
regulatory
mechanisms
human
umbilical
vein
endothelial
cells
(HUVECs)
angiogenesis
breast
remain
unknown.
Methods
We
isolated
and
characterized
cell-derived
exosomes
investigated
functions.
Exosomal
sequencing
TCGA
database
were
used
to
screen
long
non-coding
RNA
(lncRNA).
In
vitro
vivo
experiments
performed
investigate
role
exosomal
lncRNA
HUVEC
tumor
growth.
Molecular
methods
demonstrate
molecular
mechanism
lncRNA.
Results
demonstrated
that
promoted
proliferation,
tube
formation,
migration.
Combining
results
with
The
Cancer
Genome
Atlas
database,
we
screened
small
nucleolar
host
gene
12
(SNHG12),
which
was
highly
expressed
cells.
SNHG12
also
upregulated
HUVECs
co-cultured
exosome-overexpressed
SNHG12.
Moreover,
overexpression
increased
proliferation
migration,
whereas
deletion
showed
opposite
effects.
knockdown
inhibited
Transcriptome
identified
MMP10
as
target
Functional
revealed
angiogenesis.
Mechanistically,
blocked
interaction
between
PBRM1
by
directly
binding
PBRM1.
via
MMP10.
Conclusions
summary,
our
findings
confirmed
PBRM1-MMP10
axis,
leading
enhanced
malignancy
cancer.
may
be
a
novel
therapeutic
for
