The promoting effect of the POU3F2/METTL16/PFKM cascade on glycolysis and tumorigenesis of hepatocellular carcinoma
Ming Chen,
No information about this author
Yuan Yang,
No information about this author
Guangsheng Hu
No information about this author
et al.
Annals of Hepatology,
Journal Year:
2025,
Volume and Issue:
unknown, P. 101776 - 101776
Published: Jan. 1, 2025
Deregulation
of
m
Language: Английский
Emerging importance of m6A modification in liver cancer and its potential therapeutic role
Tao Chen,
No information about this author
Wufei Ye,
No information about this author
Songsen Gao
No information about this author
et al.
Biochimica et Biophysica Acta (BBA) - Reviews on Cancer,
Journal Year:
2025,
Volume and Issue:
unknown, P. 189299 - 189299
Published: March 1, 2025
Language: Английский
Hepatitis B Virus Promotes Angiogenesis in Hepatocellular Carcinoma by Increasing m6A Modification of VEGFA mRNA via IGF2BP3
Xiaoxin Xu,
No information about this author
Yi Zhang,
No information about this author
Shuxiang Wu
No information about this author
et al.
Journal of Medical Virology,
Journal Year:
2025,
Volume and Issue:
97(5)
Published: April 22, 2025
ABSTRACT
Angiogenesis
plays
a
crucial
role
in
the
development
of
HBV‐related
hepatocellular
carcinoma
(HCC).
VEGFA
is
key
angiogenic
factor,
and
while
its
transcriptional
regulation
by
HBV
has
been
extensively
studied,
posttranscriptional
remains
poorly
understood.
Building
on
our
previous
findings
that
delineated
an
RBM15/YTHDF2/IGF2BP3
regulatory
axis
m6A‐mediated
RNA
metabolism
HCC,
this
study
further
explores
HBV.
By
MeRIP‐qPCR
integrating
MeRIP‐seq
data,
we
discovered
enhances
m6A
methylation
mRNA.
Comprehensive
cellular
molecular
biology
experiments
demonstrated
induces
upregulation
IGF2BP3,
which
serves
as
“reader”
recognizes
stabilizes
mRNA
methylation‐dependent
manner.
This
stabilization
leads
to
elevated
expression,
promoting
enhanced
functions
such
HUVEC
migration
tube
formation.
Furthermore,
HBV‐associated
HCC
xenograft
model,
IGF2BP3
knockdown
resulted
decreased
expression
inhibited
tumor
growth.
expands
understanding
HBV‐driven
angiogenesis
identifies
IGF2BP3‐VEGFA
potential
therapeutic
target
for
antiangiogenic
strategies
HCC.
Language: Английский
Deciphering the IGF2BP3-mediated control of ferroptosis: mechanistic insights and therapeutic prospects
Wenjuan Zhang,
No information about this author
Hongxing Liu,
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Changrong Ren
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et al.
Discover Oncology,
Journal Year:
2024,
Volume and Issue:
15(1)
Published: Oct. 11, 2024
The
rapid
expansion
of
the
oncology
field
has
revealed
new
insights
into
cell
death
processes,
with
a
particular
emphasis
on
role
ferroptosis.
Characterized
by
iron
dependency
and
accumulation
lipid
peroxides
within
cells,
ferroptosis
stands
out
as
unique
form
programmed
demise.
This
in-depth
analysis
delves
pivotal
IGF2BP3,
an
RNA-binding
protein,
in
complex
regulatory
network
cancerous
cells.
By
exerting
post-transcriptional
control
over
genes
associated
equilibrium,
IGF2BP3
is
demonstrated
to
manage
cellular
concentrations
reactive
oxygen
species
(ROS)
thus
affecting
destiny
cell.
correlation
between
aberrant
expression
increased
aggressiveness,
metastatic
capacity,
poor
prognosis
various
cancers
further
clarified.
potential
biomarker
for
therapeutic
agent
enhance
cancer
cells'
vulnerability
also
examined,
heralding
strategies
treatment.
Language: Английский
RBM15-dependent m6A modification mediates progression of non-small cell lung cancer cells
Man Wang,
No information about this author
Ya‐Zhen Qin,
No information about this author
Xiaoqi Ai
No information about this author
et al.
Molecular Medicine,
Journal Year:
2024,
Volume and Issue:
30(1)
Published: Dec. 23, 2024
Non-small
cell
lung
cancer
(NSCLC)
is
the
predominant
form
of
cancer,
contributing
significantly
to
global
health
and
economic
challenges.
This
study
elucidated
role
RBM15
in
NSCLC
progression
through
its
involvement
m6A
modifications.
levels
tissues
cells
were
assessed
via
RT-qPCR
Western
blotting.
The
impact
knockdown
on
proliferation,
invasion,
migration
was
evaluated
using
CCK-8,
colony
formation,
Transwell
assays.
Expression
KLF1,
TRIM13,
ANXA8
determined
by
blot.
methylation
analyzed,
while
RIP
MeRIP
assays
employed
explore
interaction
between
YTHDF1/YTHDF2/m6A
KLF1/TRIM13,
as
well
KLF1
binding
promoter.
ubiquitination
examined
Xenograft
metastasis
models
utilized
assess
RBM15's
vivo.
found
be
overexpressed
NSCLC.
Silencing
led
decreased
cells.
upregulated
downregulated
TRIM13
YTHDF1/YTHDF2,
resulting
promotion
expression.
overexpression
or
downregulation
partially
reversed
suppressive
effects
proliferation.
ANXA8,
NSCLC,
mitigated
inhibitory
silencing
malignant
behaviors.
In
vivo,
hindered
proliferation
modulating
KLF1-TRIM13/ANXA8
axis.
RBM15-mediated
enhances
expression
suppresses
thereby
promoting
facilitating
progression.
These
findings
provide
novel
insights
potential
therapeutic
targets
for
treatment.
Language: Английский