bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2024,
Volume and Issue:
unknown
Published: May 17, 2024
ABSTRACT
Background
Endocrine
therapy
resistance
(ETR)
in
breast
cancer
is
achieved
via
multiple
pathways
including
a
decrease
ER,
dysregulation
of
cell
cycle
genes,
and/or
mutations
ER/co-activators/co-repressors.
We
have
reported
earlier
that
high
expression
Jumonji
domaining
containing
protein
6
(JMJD6)
induced
ETR
by
depleting
ER
expression.
In
this
study,
3
cellular
models
representing
distinct
pathways;
Tamoxifen
resistant
(TAMR),
Long-term
Estrogen
deprived
(LTEDI),
JMJD6
overexpressing
(JOE)
cells,
and
parental
MCF7
were
subjected
to
RNA-sequencing,
CNC,
ceRNA
network
analysis.
hypothesised
post-comparison
RNA
regulations
are
common
all
lines,
will
reveal
actionable
markers
targets.
These
be
shared
patients
with
ET-resistant
disease,
independent
the
initiating
event.
Results
170
differentially
expressed
genes
found,
these,
73
maintained
same
directionality
(ETR
cassette
genes).
segregated
TCGA
ER+
tumors
into
two
groups,
one
intermixing
ER-tumors.
Pathway-based
curation
identified
21
(7
up-
14
down-regulated)
participated
hallmark
pathways.
Genes
upregulated
cells
less
at
diagnosis
when
compared
normal
samples
but
their
higher
indicated
adverse
survival
outcomes.
Next,
these
used
for
CNC
construction
triad
FLT4:MIR503HG:miR-497/195/424
was
discovered.
The
levels
miRNAs
predicted
analysis
quantitative
RT-PCR
validate
down
regulation
miR-497/195/424
upregulation
targets,
FLT4
MIR503HG
cells.
Conclusions
show
total
RNA-seq
data
can
successfully
predict
achieve
drug
resistance.
Re-expression
such
as
tumor
diagnosis,
may
indicative
onset.
Finally,
arise
due
suppression
miR-424/497/195
leading
MIR503HG.
posit
suitable
target
could
developed
detection
strategy
cancer.
Taiwanese Journal of Obstetrics and Gynecology,
Journal Year:
2024,
Volume and Issue:
63(1), P. 46 - 56
Published: Jan. 1, 2024
Despite
continuous
progress
in
treatment,
recurrence
and
metastasis
limit
further
improvement
the
prognosis
of
breast
cancer
(BC)
patients.
Our
aim
was
to
search
for
a
crucial
prognostic
biomarker
BC.
Patient
data
were
selected
from
The
Cancer
Genome
Atlas
(TCGA)
GTEx
databases.
Several
online
public
databases,
including
Gene
Expression
Profiling
Interactive
Analysis
(GEPIA),
miRWalk,
miRDB,
LncBase
Predicted
v.2,
used
identify
potential
upstream
miRNAs
lncRNAs.
These
findings
validated
through
vitro
experiments.
A
total
1,
097
invasive
BC
samples
572
normal
tissues
(including
113
TCGA
459
GTEx)
collected
study.
CCT4
not
only
significantly
overexpressed
compared
with
but
also
had
important
significance
(P
<
0.001).
By
intersecting
miRWalk
miRDB
conducting
correlation
analysis,
hsa-miR-30c-2-3p
identified
as
most
probable
miRNA
CCT4.
Following
an
extensive
assessment
that
included
survival
common
binding-site
prediction,
LINC01234
chosen
likely
lncRNA.
In
experiments
showed
LINC01234-siRNA
inhibited
proliferation,
invasion,
migration
abilities
cells.
Western
blot
analysis
confirmed
promoted
malignant
behaviors
cells
via
CCT4/mTOR
signaling
pathway.
LINC01234/hsa-miR-30c-2-3p/CCT4/mTOR
axis
ceRNA
regulatory
mechanism
established
foundation
systematically
unveiling
pathological
mechanisms
provided
new
insights
targeted
therapy
Cancers,
Journal Year:
2025,
Volume and Issue:
17(2), P. 234 - 234
Published: Jan. 13, 2025
The
complex
signaling
network
within
the
breast
tumor
microenvironment
is
crucial
for
its
growth,
metastasis,
angiogenesis,
therapy
escape,
stem
cell
maintenance,
and
immunomodulation.
An
array
of
secretory
factors
their
receptors
activate
downstream
cascades
regulating
cancer
progression
metastasis.
Among
various
pathways,
EGFR,
ER,
Notch,
Hedgehog
pathways
have
recently
been
identified
as
in
terms
proliferation,
survival,
differentiation,
maintenance
CSCs,
failure.
These
mediate
such
MAPK,
including
MEK/ERK
that
promote
common
pro-oncogenic
signaling,
whereas
dysregulation
PI3K/Akt,
Wnt/β-catenin,
JAK/STAT
activates
key
oncogenic
events
drug
resistance,
CSC
enrichment,
metabolic
reprogramming.
Additionally,
these
orchestrate
an
intricate
interplay
between
stromal
cells,
immune
cells.
Metabolic
reprogramming
adaptations
contribute
to
aggressive
are
unresponsive
therapy.
Herein,
recent
insights
into
novel
operating
TME
aid
advancement
emphasized
current
developments
practices
targeting
enhance
treatment
efficacy
reviewed.
Scientific Reports,
Journal Year:
2025,
Volume and Issue:
15(1)
Published: March 22, 2025
Increased
evidence
reveals
that
glycolysis
is
one
of
the
key
metabolic
hallmarks
cancer
cells.
However,
roles
lncRNA
FTX
in
energy
metabolism
and
progression
remain
unclear.
In
this
study
we
aim
to
show
was
significantly
upregulated
tissues
serum
CRC
patients
cell
lines.
Function
indicated
it
could
promote
aerobic
glycolysis,
proliferation,
migration
invasion
colorectal
Further
mechanistic
studies
showed,
found
function
as
a
sponge
for
miR-215-3p,
which
reduced
ability
miR-215-3p
repress
YAP1
oncoprotein.
Additionally,
negative
correlation
observed
between
expression,
knockdown
or
overexpression
yielded
opposite
effects.
conclusion,
demonstrates
directly
combine
with
competitive
endogenous
RNA,
thus
promoting
vitro
vivo.
International Journal of Molecular Sciences,
Journal Year:
2025,
Volume and Issue:
26(2), P. 694 - 694
Published: Jan. 15, 2025
Long
non-coding
RNAs
(lncRNAs)
play
a
pivotal
role
in
regulating
gene
expression
and
are
critically
involved
the
progression
of
malignant
brain
tumors,
including
glioblastoma,
medulloblastoma,
meningioma.
These
lncRNAs
interact
with
microRNAs
(miRNAs),
proteins,
DNA,
influencing
key
processes
such
as
cell
proliferation,
migration,
invasion.
This
review
highlights
multifaceted
impact
lncRNA
dysregulation
on
tumor
underscores
their
potential
therapeutic
targets
to
enhance
efficacy
chemotherapy,
radiotherapy,
immunotherapy.
The
insights
provided
offer
new
directions
for
advancing
basic
research
clinical
applications
tumors.