Seminars in Cancer Biology,
Journal Year:
2020,
Volume and Issue:
83, P. 197 - 207
Published: July 29, 2020
Data
obtained
from
cutting-edge
research
have
shown
that
deregulated
epigenetic
marks
are
critical
hallmarks
of
cancer.
Rapidly
emerging
scientific
evidence
has
helped
in
developing
a
proper
understanding
the
mechanisms
leading
to
control
cellular
functions,
changes
chromatin
accessibility,
transcription
and
translation,
post-translational
modifications.
Firstly,
DNA
methylation
demethylation
introduced,
as
well
modifications
RNA,
with
particular
focus
on
N6-methyladenosine
(m6A),
discussing
effects
these
normal
cells
malignancies.
Then,
modifying
proteins
remodelling
complexes
discussed.
Many
enzymes
accessory
been
found
mutated
or
undergone
differential
splicing,
defective
protein
complexes.
Epigenetic
acting
nucleosomes
by
polycomb
repressive
SWI/SNF
nucleosome
assembly/disassembly,
main
genes
linked
cancers,
reviewed.
Among
histones
other
erasing
reversible
histone
deacetylases
(HDACs).
Sirtuins
interest
since
most
not
only
deacylate
proteins,
but
also
post-translationally
modify
adding
Mono-ADP-ribose
(MAR)
moiety.
MAR
can
be
read
MACRO-domain
containing
such
MacroH2A1,
specific
function
assembly.
Finally,
recent
advances
presented
non-coding
RNAs
scaffold
function,
prospecting
their
role
assembly
complexes,
recruiting
enzyme
players
regions.
Lastly,
imbalance
metabolites
production
due
mitochondrial
dysfunction
is
presented,
potential
inhibit
enzymes,
either
writers,
readers
erasers
epitranscriptome
marks.
In
perspectives,
studies
overwied
drugs
under
development
aiming
limit
excessive
activities
reactivate
for
therapeutic
application.
This
knowledge
may
lead
novel
personalised
medicine
cancer
patients.
Aging and Disease,
Journal Year:
2022,
Volume and Issue:
13(4), P. 970 - 970
Published: Jan. 1, 2022
Aging
is
a
major
global
challenge,
and
there
growing
demand
for
new
strategies
to
address
the
burden
of
aging.
The
intensive
search
antiaging
agents
has
led
discovery
variety
drugs
that
promote
extension
healthspan
and/or
life.
Metformin
safe,
effective,
globally
affordable
antihyperglycemic
agent
gained
much
attention
in
recent
years
as
potential
treatment.
been
shown
significantly
delay
onset
age-related
diseases
increase
lifespan
several
model
organisms.
In
this
paper,
we
reviewed
aging
hallmarks
role
metformin
countering
these
hallmarks.
We
examined
beneficial
effects
on
feasibility
an
extend
healthspan.
Finally,
discussed
research
directions
better
understand
translational
humans.
ABSTRACT
An
uninterrupted
energy
supply
is
critical
for
the
optimal
functioning
of
all
our
organs,
and
in
this
regard
human
brain
particularly
dependent.
The
study
metabolic
pathways
a
major
focus
within
neuroscience
research,
which
supported
by
genetic
defects
oxidative
phosphorylation
mechanism
often
contributing
towards
neurodevelopmental
disorders
changes
glucose
metabolism
presenting
as
hallmark
feature
age-dependent
neurodegenerative
disorders.
However,
recent
studies
have
illuminated
roles
cellular
that
span
far
beyond
mere
energetics,
it
would
be
valuable
to
first
comprehend
physiological
involvement
neural
cell
fate
function,
subsequently
reconstruct
their
impact
on
diseases
brain.
In
Review,
we
discuss
evidence
implies
master
regulator
identity
during
development.
Additionally,
examine
type-dependent
states
present
adult
As
been
studied
extensively
crucial
regulators
malignant
transformation
cancer,
reveal
how
knowledge
gained
from
field
cancer
has
aided
understanding
likewise
controls
determination
stability
directly
wiring
into
epigenetic
landscape.
We
further
summarize
research
pertaining
interplay
between
alterations
psychiatric
disorders,
expose
an
improved
control
might
assist
development
new
concepts
combat
diseases,
Alzheimer's
disease.
Aging,
Journal Year:
2023,
Volume and Issue:
unknown
Published: April 20, 2023
The
World
Health
Organization
predicts
that
by
2050,
2.1
billion
people
worldwide
will
be
over
60
years
old,
a
drastic
increase
from
only
1
in
2019.
Considering
these
numbers,
strategies
to
ensure
an
extended
"healthspan"
or
healthy
longevity
are
urgently
needed.
present
study
approaches
the
promotion
of
healthspan
epigenetic
perspective.
Epigenetic
phenomena
modifiable
response
individual's
environmental
exposures,
and
therefore
link
environment
their
gene
expression
pattern.
studies
demonstrate
aging
is
associated
with
decondensation
chromatin,
leading
altered
heterochromatin
structure,
which
promotes
accumulation
errors.
In
this
review,
we
describe
how
impacts
epigenetics
nutrition
physical
exercise
can
positively
impact
process,
point
view.
Canonical
histones
replaced
histone
variants,
concomitant
post-translational
modifications.
A
slight
DNA
methylation
at
promoters
has
been
observed,
represses
transcription
previously
active
genes,
parallel
global
genome
hypomethylation.
Aging
also
deregulation
-
usually
provided
non-coding
RNAs
both
repression
transcribed
genes
repressed
genes.
Age-associated
events
less
common
individuals
lifestyle,
including
balanced
nutrition,
caloric
restriction
exercise.
Healthy
more
tightly
condensed
fewer
PTMs
greater
regulation
ncRNAs.
Cellular and Molecular Life Sciences,
Journal Year:
2021,
Volume and Issue:
78(7), P. 3141 - 3158
Published: Jan. 28, 2021
Regulation
of
the
differentiated
identity
requires
active
and
continued
supervision.
Inability
to
maintain
state
is
a
hallmark
aging
aging-related
disease.
To
cellular
identity,
network
nuclear
regulators
devoted
silencing
previous
non-relevant
gene
programs.
This
involves
transcription
factors,
epigenetic
regulators,
localization
silent
genes
heterochromatin.
Together,
supervisors
mold
unique
environment
cell.
review
describes
recent
discoveries
regarding
mechanisms
that
supervise
protect
from
de-differentiation,
tumorigenesis,
attenuate
forced
somatic
cell
reprograming.
The
focuses
on
involved
in
H3K9me3-decorated
heterochromatin
importance
lamins
identity.
We
outline
how
biophysical
properties
these
factors
are
self-compartmentalization
Finally,
we
discuss
relevance
age-related
Journal of Biological Chemistry,
Journal Year:
2025,
Volume and Issue:
unknown, P. 108271 - 108271
Published: Feb. 1, 2025
Hyperglycemia
is
a
hallmark
of
metabolic
disorders,
yet
the
precise
mechanisms
linking
epigenetic
regulation
to
glucose
metabolism
remain
underexplored.
Coactivator-associated
arginine
methyltransferase
1
(CARM1),
type
I
histone
methyltransferase,
promotes
transcriptional
activation
through
methylation
H3
at
residues
H3R17
and
H3R26.
Here,
we
identify
novel
mechanism
by
which
metformin,
widely
prescribed
antidiabetic
drug,
inhibits
CARM1
activity.
Using
biochemical
biophysical
assays,
show
that
metformin
binds
substrate-binding
site
CARM1,
reducing
levels
in
CARM1-overexpressing
hepatic
cells
liver
tissues
from
metformin-fed
mice.
This
modulation
suppresses
expression
gluconeogenic
enzymes
(G6Pase,
FBPase,
PCK1),
thereby
reversing
CARM1-induced
glycolytic
suppression
regulating
gluconeogenesis.
Importantly,
does
not
alter
protein
its
recruitment
gene
promoters
but
diminishes
H3R17me2a
marks
these
loci.
Our
findings
reveal
previously
unrecognized
action,
offering
new
therapeutic
insights
for
hyperglycemia
management.
Psychiatric Genetics,
Journal Year:
2025,
Volume and Issue:
unknown
Published: March 21, 2025
Although
psychotic
symptoms
have
occasionally
been
associated
with
pathogenic
CHD2
variants,
few
articles
provided
phenotypic
information
in
this
respect
or
described
treatment
response.
We
describe
an
18-year-old
female
a
15q26.1
interstitial
deletion
that
disrupts
CHD2,
who
at
age
12
developed
variety
of
responded
well
to
quetiapine
therapy.
She
also
exhibited
improvement
her
cognitive
functioning,
language
skills,
and
social
responsiveness,
which
coincided
the
initiation
metformin.
This
is
only
third
report
characterize
antipsychotic
response
individual
harboring
variant,
first
do
so
relation
quetiapine.
anecdotal,
develop
variants
may
respond
atypical
therapy,
metformin
additional
benefits
population
behavioral/social
deficits.
However,
more
evidence
needed
before
any
firm
conclusions
can
be
drawn.
