Redox Biology,
Journal Year:
2020,
Volume and Issue:
37, P. 101697 - 101697
Published: Aug. 28, 2020
Ferroptosis
is
a
newly
defined
form
of
cell
death
induced
by
iron-dependent
accumulation
lethal
lipid
peroxidation.
represent
therapeutic
strategy
to
suppress
therapy-resistant
cancer
cells
with
more
property
epithelial-mesenchymal
transition
(EMT).
However,
epigenetic
reprogramming
EMT
has
been
rarely
studied
in
the
context
ferroptosis
susceptibility.
Therefore,
we
examined
potentiality
promoting
head
and
neck
(HNC)
cells.
The
effects
inducers
inhibition
or
induction
were
tested
HNC
lines
mouse
tumor
xenograft
models.
These
analyzed
concerning
viability
death,
reactive
oxygen
species
iron
production,
labile
pool,
glutathione
contents,
NAD/NADH
levels,
mRNA/protein
expression.
Cell
density
expression
levels
E-cadherin,
vimentin,
ZEB1
associated
different
susceptibility
inducers.
CDH1
silencing
overexpression
increased
ferroptosis,
whereas
CDH
decreased
susceptibility,
vitro
vivo.
Histone
deacetylase
SIRT1
gene
pharmacological
EX-527
suppressed
consequently
SIRT
inducers,
resveratrol
SRT1720,
ferroptosis.
MiR-200
family
inhibitors
In
low
treatment
5-azacitidine
diminished
hypermethylation
CDH1,
resulting
E-cadherin
Our
data
suggest
that
contributes
Cold Spring Harbor Perspectives in Biology,
Journal Year:
2017,
Volume and Issue:
10(4), P. a022293 - a022293
Published: April 21, 2017
Kevin
K.
Kim1,
Dean
Sheppard2
and
Harold
A.
Chapman2
1Department
of
Medicine,
University
Michigan
School
Ann
Arbor,
48109
2Department
Cardiovascular
Research
Institute,
Lung
Biology
Center,
California,
San
Francisco,
California
94143
Correspondence:
hal.chapman{at}ucsf.edu
Journal of Cellular Physiology,
Journal Year:
2017,
Volume and Issue:
232(12), P. 3261 - 3272
Published: Jan. 13, 2017
The
lineage
transition
between
epithelium
and
mesenchyme
is
a
process
known
as
epithelial–mesenchymal
(EMT),
by
which
polarized
epithelial
cells
lose
their
adhesion
property
obtain
mesenchymal
cell
phenotypes.
EMT
biological
that
often
involved
in
embryogenesis
diseases,
such
cancer
invasion
metastasis.
the
reverse
process,
mesenchymal–epithelial
(MET),
also
play
important
roles
stem
differentiation
de‐differentiation
(or
reprogramming).
In
this
review,
we
will
discuss
current
research
progress
of
embryonic
development,
cellular
reprogramming,
progression,
all
are
representative
models
for
researches
biology
normal
diseases.
Understanding
MET
may
help
to
identify
specific
markers
distinguish
from
future.
Journal of Clinical Medicine,
Journal Year:
2016,
Volume and Issue:
5(5), P. 51 - 51
Published: April 29, 2016
Tumor
budding
is
a
histological
phenomenon
encountered
in
various
cancers,
whereby
individual
malignant
cells
and/or
small
clusters
of
are
seen
the
tumor
stroma.
Postulated
to
be
mirror
epithelial-mesenchymal
transition,
has
been
associated
with
poor
cancer
outcomes.
However,
vast
heterogeneity
its
exact
definition,
methodology
assessment,
and
patient
stratification
need
resolved
before
it
can
routinely
used
as
standardized
prognostic
feature.
Here,
we
discuss
defining
assessing
budding,
clinical
significance
across
multiple
types,
prospective
implementation
practice.
Next,
review
emerging
evidence
about
partial,
rather
than
complete,
phenotype
at
bud
level,
connection
proliferation,
quiescence,
stemness.
Finally,
based
on
recent
literature,
indicating
co-expression
epithelial
mesenchymal
markers
many
buds,
posit
manifestation
this
hybrid
epithelial/mesenchymal
displaying
collective
cell
migration.
Proceedings of the National Academy of Sciences,
Journal Year:
2019,
Volume and Issue:
116(15), P. 7353 - 7362
Published: March 25, 2019
Carcinoma
cells
residing
in
an
intermediate
phenotypic
state
along
the
epithelial–mesenchymal
(E–M)
spectrum
are
associated
with
malignant
phenotypes,
such
as
invasiveness,
tumor-initiating
ability,
and
metastatic
dissemination.
Using
recently
described
CD104
+
/CD44
hi
antigen
marker
combination,
we
isolated
highly
tumorigenic
breast
cancer
stably—both
vitro
vivo—in
coexpressing
both
epithelial
(E)
mesenchymal
(M)
markers.
We
demonstrate
that
tumorigenicity
depends
on
individual
this
E/M
hybrid
cannot
be
phenocopied
by
mixing
two
cell
populations
reside
stably
at
ends
of
spectrum,
i.e.,
E
M
state.
Hence,
residence
a
specific
E–M
rather
than
plasticity
appears
critical
to
expression
capacity.
Acquisition
is
facilitated
differential
EMT-inducing
transcription
factors
(EMT-TFs)
accompanied
adult
stem
programs,
notably,
active
canonical
Wnt
signaling.
Furthermore,
transition
from
fully
phenotype,
achieved
constitutive
ectopic
Zeb1,
sufficient
drive
out
into
state,
which
substantial
loss
switch
noncanonical
Identifying
gatekeepers
various
states
arrayed
likely
prove
useful
developing
therapeutic
approaches
operate
shifting
between
distinct
spectrum.
