Translational Oncology,
Journal Year:
2024,
Volume and Issue:
41, P. 101860 - 101860
Published: Jan. 22, 2024
Nutrient
restriction
in
cancer
cells
can
activate
a
number
of
stress
response
pathways
for
cell
survival.
We
aimed
to
determine
mechanistically
how
nutrient
depletion
colorectal
(CRC)
leads
cellular
adaptation.
Cell
survival
under
(ND)
was
evaluated
by
colony
formation
and
vivo
tumor
assays.
Lysosomes
are
activated
with
ND;
therefore,
we
incubated
the
ND
V-ATPase
inhibitor
Bafilomycin
A1
(ND+Baf).
The
expression
epithelial
mesenchymal
markers
ND+Baf
determined
RNA
sequencing
RT-qPCR
while
motility
an
Chorioallantoic
membrane
(CAM)
assay.
Reorganization
cytoskeletal
network
lysosomal
positioning
immunocytochemistry.
4
different
lines
showed
high
viability,
forming
ability
increased
one
or
more
markers,
suggesting
activation
partial
(p)-EMT.
observed
further
increase
p-EMT
numerous
protrusions,
decreased
cell-cell
adhesion
3D,
cells.
protrusions
were
primarily
mediated
microtubules
enabled
relocalization
lysosomes
from
perinuclear
region
periphery.
CRC
cells,
which
exacerbated
alkalinization.
also
containing
lysosomes,
may
lead
exocytosis
enhanced
motility.
Frontiers in Cell and Developmental Biology,
Journal Year:
2025,
Volume and Issue:
13
Published: March 11, 2025
Lysosomes
are
heterogeneous,
acidic
organelles
whose
proper
functionality
is
critically
dependent
on
maintaining
the
integrity
of
their
membranes
and
acidity
within
lumen.
When
subjected
to
stress,
lysosomal
membrane
can
become
permeabilized,
posing
a
significant
risk
organelle’s
survival
necessitating
prompt
repair.
Although
numerous
mechanisms
for
repair
have
been
identified
in
recent
years,
progression
lysosome-related
diseases
more
closely
linked
alternative
strategies
when
fail,
particularly
contexts
aging
pathogen
infection.
This
review
explores
responses
damage,
including
secretion
contents
interactions
with
lysosome-associated
endolysosomal
system.
Furthermore,
it
examines
role
outside
this
system,
such
as
endoplasmic
reticulum
(ER)
Golgi
apparatus,
auxiliary
These
crucial
understanding
disease
progression.
For
instance,
spread
misfolded
proteins
play
key
roles
neurodegenerative
advancement,
while
escape
via
lysosomotropic
drug
expulsion
underlie
cancer
treatment
resistance.
Reexamining
these
fallback
could
provide
new
perspectives
biology
contribution
Translational Oncology,
Journal Year:
2024,
Volume and Issue:
41, P. 101860 - 101860
Published: Jan. 22, 2024
Nutrient
restriction
in
cancer
cells
can
activate
a
number
of
stress
response
pathways
for
cell
survival.
We
aimed
to
determine
mechanistically
how
nutrient
depletion
colorectal
(CRC)
leads
cellular
adaptation.
Cell
survival
under
(ND)
was
evaluated
by
colony
formation
and
vivo
tumor
assays.
Lysosomes
are
activated
with
ND;
therefore,
we
incubated
the
ND
V-ATPase
inhibitor
Bafilomycin
A1
(ND+Baf).
The
expression
epithelial
mesenchymal
markers
ND+Baf
determined
RNA
sequencing
RT-qPCR
while
motility
an
Chorioallantoic
membrane
(CAM)
assay.
Reorganization
cytoskeletal
network
lysosomal
positioning
immunocytochemistry.
4
different
lines
showed
high
viability,
forming
ability
increased
one
or
more
markers,
suggesting
activation
partial
(p)-EMT.
observed
further
increase
p-EMT
numerous
protrusions,
decreased
cell-cell
adhesion
3D,
cells.
protrusions
were
primarily
mediated
microtubules
enabled
relocalization
lysosomes
from
perinuclear
region
periphery.
CRC
cells,
which
exacerbated
alkalinization.
also
containing
lysosomes,
may
lead
exocytosis
enhanced
motility.
