Cell Reports,
Journal Year:
2018,
Volume and Issue:
22(3), P. 569 - 575
Published: Jan. 1, 2018
How
cancer
cells
respond
to
nutrient
deprivation
remains
poorly
understood.
In
certain
cells,
of
cystine
induces
a
non-apoptotic,
iron-dependent
form
cell
death
termed
ferroptosis.
Recent
evidence
suggests
that
ferroptosis
sensitivity
may
be
modulated
by
the
stress-responsive
transcription
factor
and
canonical
tumor
suppressor
protein
p53.
Using
CRISPR/Cas9
genome
editing,
small-molecule
probes,
high-resolution,
time-lapse
imaging,
we
find
stabilization
wild-type
p53
delays
onset
in
response
deprivation.
This
delay
requires
transcriptional
target
CDKN1A
(encoding
p21)
is
associated
with
both
slower
depletion
intracellular
glutathione
reduced
accumulation
toxic
lipid-reactive
oxygen
species
(ROS).
Thus,
p53-p21
axis
help
cope
metabolic
stress
induced
delaying
non-apoptotic
death.
Frontiers in Cell and Developmental Biology,
Journal Year:
2021,
Volume and Issue:
9
Published: March 29, 2021
Cellular
senescence
is
a
stable
cell
cycle
arrest
that
can
be
triggered
in
normal
cells
response
to
various
intrinsic
and
extrinsic
stimuli,
as
well
developmental
signals.
Senescence
considered
highly
dynamic,
multi-step
process,
during
which
the
properties
of
senescent
continuously
evolve
diversify
context
dependent
manner.
It
associated
with
multiple
cellular
molecular
changes
distinct
phenotypic
alterations,
including
proliferation
unresponsive
mitogenic
stimuli.
Senescent
remain
viable,
have
alterations
metabolic
activity
undergo
dramatic
gene
expression
develop
complex
senescence-associated
secretory
phenotype.
compromise
tissue
repair
regeneration,
thereby
contributing
toward
aging.
Removal
attenuate
age-related
dysfunction
extend
health
span.
also
act
potent
anti-tumor
mechanism,
by
preventing
potentially
cancerous
cells.
program
acts
double-edged
sword,
both
beneficial
detrimental
effects
on
organism,
an
example
evolutionary
antagonistic
pleiotropy.
Activation
p53/p21
WAF1/CIP1
p16
INK4A
/pRB
tumor
suppressor
pathways
play
central
role
regulating
senescence.
Several
other
recently
been
implicated
mediating
Herein
we
review
mechanisms
underlie
growth
particular
focus
why
stop
dividing,
stability
arrest,
hypersecretory
phenotype
how
different
are
all
integrated.
The Journal of Cell Biology,
Journal Year:
2017,
Volume and Issue:
217(1), P. 65 - 77
Published: Nov. 7, 2017
Aging
is
the
major
risk
factor
for
cancer,
cardiovascular
disease,
diabetes,
and
neurodegenerative
disorders.
Although
we
are
far
from
understanding
biological
basis
of
aging,
research
suggests
that
targeting
aging
process
itself
could
ameliorate
many
age-related
pathologies.
Senescence
a
cellular
response
characterized
by
stable
growth
arrest
other
phenotypic
alterations
include
proinflammatory
secretome.
plays
roles
in
normal
development,
maintains
tissue
homeostasis,
limits
tumor
progression.
However,
senescence
has
also
been
implicated
as
cause
disease.
In
this
regard,
recent
experimental
evidence
shown
genetic
or
pharmacological
ablation
senescent
cells
extends
life
span
improves
health
span.
Here,
review
molecular
links
between
discuss
novel
therapeutic
avenues
connection
opens.
Oncogenesis,
Journal Year:
2018,
Volume and Issue:
7(1)
Published: Jan. 22, 2018
Cancer
progression
often
benefits
from
the
selective
conditions
present
in
tumour
microenvironment,
such
as
presence
of
cancer-associated
fibroblasts
(CAFs),
deregulated
ECM
deposition,
expanded
vascularisation
and
repression
immune
response.
Generation
a
hypoxic
environment
activation
its
main
effector,
hypoxia-inducible
factor-1
(HIF-1),
are
common
features
advanced
cancers.
In
addition
to
impact
on
cell
biology,
influence
that
hypoxia
exerts
surrounding
cells
represents
critical
step
tumorigenic
process.
Hypoxia
indeed
enables
number
events
microenvironment
lead
expansion
aggressive
clones
heterogeneous
promote
lethal
phenotype.
this
article,
we
review
most
relevant
findings
describing
contribution
HIF
major
components
summarise
their
role
cancer
development
progression.
