Genes to Cells,
Год журнала:
2024,
Номер
29(11), С. 1012 - 1025
Опубликована: Окт. 2, 2024
Abstract
Regular
exercise
is
believed
to
suppress
cancer
progression.
However,
the
precise
molecular
mechanisms
by
which
prevents
development
remain
unclear.
In
this
study,
using
a
steatosis‐associated
liver
mouse
model,
we
found
that
regular
at
speed
of
18
m/min
for
20
min
daily
suppressed
development.
To
explore
underlying
mechanisms,
examined
gene
expression
profiles
in
livers
and
non‐exercise
groups.
The
expressions
circadian
genes,
such
as
Per1
Cry2,
were
upregulated
group.
As
rhythm
disruption
known
cause
various
diseases,
including
cancer,
improving
through
could
contribute
prevention.
We
further
series
E2F1
c‐Myc
target
genes
directly
affect
proliferation
cells
was
downregulated
transcriptionally
unchanged
but
degraded
post‐translational
level
exercise.
regulated
Skp1‐Cul1‐FBXL3
(SCF
FBXL3
)
ubiquitin
ligase
complex
binding
FBXL3,
can
form
with
c‐Myc,
think
mechanism
degrade
them.
Our
study
revealed
previously
unknown
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(20), С. 10926 - 10926
Опубликована: Окт. 11, 2024
Circadian
rhythms,
the
internal
timekeeping
systems
governing
physiological
processes,
significantly
influence
skin
health,
particularly
in
response
to
ultraviolet
radiation
(UVR).
Disruptions
circadian
rhythms
can
exacerbate
UVR-induced
damage
and
increase
risk
of
aging
cancer.
This
review
explores
how
affect
various
aspects
physiology
pathology,
with
a
special
focus
on
DNA
repair.
regulation
ensures
optimal
repair
following
damage,
reducing
mutation
accumulation,
enhancing
genomic
stability.
The
control
over
cell
proliferation
apoptosis
further
contributes
regeneration
UVR.
Oxidative
stress
management
is
another
critical
area
where
exert
influence.
Key
genes
like
brain
muscle
ARNT-like
1
(BMAL1)
locomotor
output
cycles
kaput
(CLOCK)
modulate
activity
antioxidant
enzymes
signaling
pathways
protect
cells
from
oxidative
stress.
also
inflammatory
immune
responses
by
modulating
Langerhans
other
skin.
In
summary,
form
complex
defense
network
that
manages
through
precise
repair,
proliferation,
apoptosis,
response,
stress,
hormonal
signaling.
Understanding
these
mechanisms
provides
insights
into
developing
targeted
protection
improving
cancer
prevention.
ABSTRACT
Background
Circadian
rhythms
are
approximately
24‐hour
cycles
in
physiological
and
behavioral
processes.
They
entrained
to
the
external
solar
day
via
blue
wavelength
light.
Disruptions
these
intrinsic
can
lead
circadian
dysfunction,
which
has
several
negative
implications
on
human
health,
including
cancer
development
progression.
Aims
Here
we
review
molecular
mechanisms
of
disruption
their
impact
tumor
progression,
discuss
interplay
between
dysfunction
basic
scientific
studies
clinical
data,
propose
potential
data
that
may
be
used
improve
patient
outcomes
reduce
cost
treatment.
Materials
&
Methods
Using
literature
databases,
relevant
were
analyzed
draw
overarching
conclusions
relationship
rhythm
dysruption
cancer.
Conclusions
mediated
by
a
number
environmental
factors
such
as
exposure
light
at
night,
shift
work,
jetlag,
social
jetlag
drive
oncogenesis.
Tumor
growth
well
treatment,
long‐term
alterations
negatively
affect
quality
life
survivors.
Genes to Cells,
Год журнала:
2024,
Номер
29(11), С. 1012 - 1025
Опубликована: Окт. 2, 2024
Abstract
Regular
exercise
is
believed
to
suppress
cancer
progression.
However,
the
precise
molecular
mechanisms
by
which
prevents
development
remain
unclear.
In
this
study,
using
a
steatosis‐associated
liver
mouse
model,
we
found
that
regular
at
speed
of
18
m/min
for
20
min
daily
suppressed
development.
To
explore
underlying
mechanisms,
examined
gene
expression
profiles
in
livers
and
non‐exercise
groups.
The
expressions
circadian
genes,
such
as
Per1
Cry2,
were
upregulated
group.
As
rhythm
disruption
known
cause
various
diseases,
including
cancer,
improving
through
could
contribute
prevention.
We
further
series
E2F1
c‐Myc
target
genes
directly
affect
proliferation
cells
was
downregulated
transcriptionally
unchanged
but
degraded
post‐translational
level
exercise.
regulated
Skp1‐Cul1‐FBXL3
(SCF
FBXL3
)
ubiquitin
ligase
complex
binding
FBXL3,
can
form
with
c‐Myc,
think
mechanism
degrade
them.
Our
study
revealed
previously
unknown
