Dichotomous roles of ACBD3 in NSCLC growth and metastasis
Oncogene,
Journal Year:
2025,
Volume and Issue:
unknown
Published: April 6, 2025
Abstract
Lung
cancer
continues
to
be
the
leading
cause
of
cancer-related
deaths
globally.
Unraveling
regulators
behind
lung
growth
and
its
metastatic
spread,
along
with
understanding
underlying
mechanisms,
is
crucial
for
developing
novel
effective
therapeutic
strategies.
While
much
research
has
focused
on
identifying
potential
oncogenes
or
tumor
suppressors,
roles
certain
genes
can
vary
depending
context
may
even
exhibit
contradictory
effects.
In
this
study,
we
demonstrate
that
acyl-CoA
binding
domain
containing
3
(ACBD3),
a
Golgi
resident
protein,
promotes
primary
by
recruiting
phosphatidylinositol
(PI)-4-kinase
IIIβ
(PI4KB)
Golgi,
thereby
enhancing
oncogenic
secretion
in
chromosome
1q-amplified
cells.
Conversely,
1q-diploid
cells,
ACBD3
acts
as
suppressor
metastasis
inhibiting
NOTCH
signaling
pathway
reducing
cell
motility.
This
highlights
intricacy
progression
cautions
against
simplistic
approaches
targeting
individual
therapy.
Language: Английский
Targeting the secretory program of 3q-amplified lung cancers
Journal of Clinical Investigation,
Journal Year:
2024,
Volume and Issue:
134(12)
Published: June 16, 2024
Designing
strategies
to
target
cell
proliferation
has
been
a
priority
of
cancer
researchers
for
decades.
However,
targeting
the
secretory
programs
transformed
cells
can
influence
other
features
such
as
survival,
migration,
and
communication
with
tumor
stroma.
In
this
issue
JCI,
Tan
colleagues
describe
functional
cooperativity
between
Golgi-resident
proteins
Golgi
integral
membrane
protein
4
(GOLIM4)
ATPase
pathway
Ca2+
transporting
1
(ATP2C1)
in
coordination
program
3q-amplified
cancers.
Targeting
these
tumors
manganese
(Mn2+)
promoted
GOLIM4
degradation
imposed
blockade
that
impaired
progression
stromal
recruitment
mice.
These
findings
highlight
therapeutic
malignancies
provide
promising
strategy
treat
progression.
Language: Английский
The cancer-associated secretory phenotype: a new frontier in targeted therapeutics
Journal of Clinical Investigation,
Journal Year:
2024,
Volume and Issue:
134(17)
Published: Sept. 2, 2024
Language: Английский
IRE1-dependent GOLIM4 expression controls protein secretion to modulate glioblastoma cell adhesion and migration
Ketsia Bakambamba,
No information about this author
Manon Nivet,
No information about this author
Chloé Sauzay
No information about this author
et al.
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2024,
Volume and Issue:
unknown
Published: Oct. 25, 2024
Abstract
One
of
the
main
glioblastoma
(GB)
features
is
diffuse
migration
tumor
cells
within
surrounding
brain
parenchyma,
rendering
almost
impossible
complete
resection
and
irradiation,
leading
to
inexorable
lethal
relapse
disease.
In
past
years,
we
demonstrated
that
IRE1α
(hereafter
IRE1),
one
Endoplasmic
Reticulum
(ER)
stress
sensors,
plays
a
key
role
in
GB
biology
by
impacting
on
immune
infiltration,
angiogenesis
cell
migration/invasion,
all
these
being
linked
an
alteration
protein
secretion.
present
study,
investigated
if
how
IRE1
could
regulate
functionality
secretory
machinery
identified
GOLIM4,
Golgi-associated
molecule
whose
expression
regulated
downstream
through
transcription
XBP1s.
Interestingly,
GOLIM4
silencing
led
decreased
surface
multiple
molecules
including
MHC
class
I
molecules,
growth
factor
receptors
(PDGFRA
IL13RA2)
proteins
involved
cell-cell
adhesion
(CD44,
CD54,
NCAM1),
matrix
(ITGB1)
or
(CD90)
without
their
encoding
transcripts’
levels.
Moreover,
phenotypically
affected
models.
Overall,
have
described
novel
IRE1/XBP1s/GOLIM4
operon
controls
secretion
specific
impacts
aggressiveness.
Graphical
abstract
Language: Английский