Scientific Reports,
Journal Year:
2024,
Volume and Issue:
14(1)
Published: March 24, 2024
Abstract
It
is
metabolic
and
signaling
crosstalk
between
stromal
cells
tumors
in
the
tumor
microenvironment,
which
influences
several
aspects
of
formation
drug
resistance,
including
reprogramming.
Despite
considerable
findings
linking
lncRNAs
HIF-1-related
regulatory
networks
to
cancer
cell,
little
emphasis
has
been
given
role
communication
cancer-associated
fibroblasts
(CAFs)
cells.
Previously,
we
observed
that
NNT-AS1
was
substantially
expressed
CAFs
exosomes,
subsequently
investigated
influence
exosomal
on
glucose
metabolism,
proliferation,
metastasis
pancreatic
ductal
adenocarcinoma
(PDAC)
Transmission
electron
microscopy
used
examine
exosomes
secreted
by
PDAC
patient-derived
CAFs.
qRT-PCR
evaluate
expression
NNT-AS1,
miR-889-3p,
HIF-1.
The
CAFs-derived
cell
progression
metabolism
have
identified.
Dual
luciferase
reporter
assays
examined
binding
After
co-culture
CAFs,
found
they
alter
metastasis.
In
cells,
CAF-derived
lncRNA
acted
as
a
molecular
sponge
for
miR-889-3p.
Furthermore,
HIF-1
could
be
targeted
miR-889-3p
controlled
NNT-AS1.
This
study
explores
mechanism
interaction
glycolytic
remodeling,
through
regulating
miR-889-3p/HIF-1α,
also
helps
discover
new
clinical
treatment
targets
PDAC.
Frontiers in Oncology,
Journal Year:
2024,
Volume and Issue:
14
Published: April 2, 2024
Hepatocellular
carcinoma
(HCC)
is
the
most
common
primary
malignant
liver
tumor
and
one
of
leading
causes
cancer-related
deaths
worldwide.
The
Wnt/β-Catenin
signaling
pathway
a
highly
conserved
involved
in
several
biological
processes,
including
improper
regulation
that
leads
to
tumorigenesis
progression
cancer.
New
studies
have
found
abnormal
activation
major
cause
HCC
tumorigenesis,
progression,
resistance
therapy.
perspectives
approaches
treating
will
arise
from
understanding
this
pathway.
This
article
offers
thorough
analysis
pathway’s
function
its
therapeutic
implications
HCC.
Journal of Biomedical Science,
Journal Year:
2024,
Volume and Issue:
31(1)
Published: Feb. 26, 2024
Abstract
Breast
cancer
is
one
of
the
most
common
malignancies
that
pose
a
serious
threat
to
women's
health.
Reprogramming
energy
metabolism
major
feature
malignant
transformation
breast
cancer.
Compared
normal
cells,
tumor
cells
reprogram
metabolic
processes
more
efficiently,
converting
nutrient
supplies
into
glucose,
amino
acid
and
lipid
required
for
proliferation
progression.
Non-coding
RNAs(ncRNAs)
are
class
functional
RNA
molecules
not
translated
proteins
but
regulate
expression
target
genes.
NcRNAs
have
been
demonstrated
be
involved
in
various
aspects
metabolism,
including
glycolysis,
glutaminolysis,
fatty
synthesis.
This
review
focuses
on
regulatory
mechanisms
clinical
applications
metabolism-regulating
ncRNAs
We
summarize
vital
roles
played
by
endocrine
therapy,
targeted
chemotherapy,
immunotherapy,
radiotherapy
resistance
cancer,
as
well
their
potential
therapeutic
targets
biomarkers.
Difficulties
perspectives
current
non-coding
strategies
discussed.
Scientific Reports,
Journal Year:
2024,
Volume and Issue:
14(1)
Published: March 24, 2024
Abstract
It
is
metabolic
and
signaling
crosstalk
between
stromal
cells
tumors
in
the
tumor
microenvironment,
which
influences
several
aspects
of
formation
drug
resistance,
including
reprogramming.
Despite
considerable
findings
linking
lncRNAs
HIF-1-related
regulatory
networks
to
cancer
cell,
little
emphasis
has
been
given
role
communication
cancer-associated
fibroblasts
(CAFs)
cells.
Previously,
we
observed
that
NNT-AS1
was
substantially
expressed
CAFs
exosomes,
subsequently
investigated
influence
exosomal
on
glucose
metabolism,
proliferation,
metastasis
pancreatic
ductal
adenocarcinoma
(PDAC)
Transmission
electron
microscopy
used
examine
exosomes
secreted
by
PDAC
patient-derived
CAFs.
qRT-PCR
evaluate
expression
NNT-AS1,
miR-889-3p,
HIF-1.
The
CAFs-derived
cell
progression
metabolism
have
identified.
Dual
luciferase
reporter
assays
examined
binding
After
co-culture
CAFs,
found
they
alter
metastasis.
In
cells,
CAF-derived
lncRNA
acted
as
a
molecular
sponge
for
miR-889-3p.
Furthermore,
HIF-1
could
be
targeted
miR-889-3p
controlled
NNT-AS1.
This
study
explores
mechanism
interaction
glycolytic
remodeling,
through
regulating
miR-889-3p/HIF-1α,
also
helps
discover
new
clinical
treatment
targets
PDAC.