Scientific Reports,
Journal Year:
2025,
Volume and Issue:
15(1)
Published: Feb. 25, 2025
Abstract
Identifying
specific
inhibitors
of
the
MYC
oncogene
has
been
challenging,
due
to
off
target
effects
associated
with
inhibition.
This
study
investigated
how
recombinant
Escherichia
coli
Lon
protease
(rLon),
which
targets
in
human
cells,
inhibits
over-activation
models
infection
and
cancer.
In
silico
predictions
identified
peptide
domains
bacterial
that
affinity
these
peptides
for
was
by
surface
plasmon
resonance.
The
N-terminal
domain
rLon
shown
interact
C-terminal,
leucine
zipper
MAX
prevent
MYC/MAX
dimerization.
Furthermore,
targeted
degraded
c-MYC
vitro
cellular
models,
through
peptidase
domain.
a
model
kidney
infection,
treatment
prevented,
c-MYC,
N-MYC
L-MYC
over-expression,
MYC-dependent
gene
expression,
specifically
renal
toxicity
genes
pathology,
suggesting
recognizes
corrects
dysregulation
this
disease.
findings
describe
multitarget
mechanism
inhibition
rLon,
combined
achieved
domains,
targeting
different
epitopes
functions,
no
evidence
or
detrimental
on
homeostatic
expression.
Journal of Hematology & Oncology,
Journal Year:
2021,
Volume and Issue:
14(1)
Published: Nov. 17, 2021
Abstract
The
multipotent
mesenchymal
stem/stromal
cells
(MSCs),
initially
discovered
from
bone
marrow
in
1976,
have
been
identified
nearly
all
tissues
of
human
body
now.
multipotency
MSCs
allows
them
to
give
rise
osteocytes,
chondrocytes,
adipocytes,
and
other
lineages.
Moreover,
armed
with
the
immunomodulation
capacity
tumor-homing
property,
are
special
relevance
for
cell-based
therapies
treatment
cancer.
However,
hampered
by
lack
knowledge
about
controversial
roles
that
MSC
plays
crosstalk
tumors,
limited
progress
has
made
regard
translational
medicine.
Therefore,
this
review,
we
discuss
prospects
MSC-associated
anticancer
strategies
light
therapeutic
mechanisms
signal
transduction
pathways.
In
addition,
clinical
trials
designed
appraise
efficacy
safety
MSC-based
will
be
assessed
according
published
data.
Journal of Hematology & Oncology,
Journal Year:
2021,
Volume and Issue:
14(1)
Published: Aug. 9, 2021
Abstract
MYC
oncogene
is
a
transcription
factor
with
wide
array
of
functions
affecting
cellular
activities
such
as
cell
cycle,
apoptosis,
DNA
damage
response,
and
hematopoiesis.
Due
to
the
multi-functionality
MYC,
its
expression
regulated
at
multiple
levels.
Deregulation
this
can
give
rise
variety
cancers.
In
review,
regulation
mechanisms
by
which
adjusts
implication
in
hematologic
malignancies
are
summarized.
Further,
we
also
discuss
potential
inhibitors
that
could
be
beneficial
for
treating
malignancies.
Aging and Disease,
Journal Year:
2024,
Volume and Issue:
15(2), P. 640 - 640
Published: Jan. 1, 2024
Various
diseases,
including
cancers,
age-associated
disorders,
and
acute
liver
failure,
have
been
linked
to
the
oncogene,
MYC.
Animal
testing
clinical
trials
shown
that
sustained
tumor
volume
reduction
can
be
achieved
when
MYC
is
inactivated,
different
combinations
of
therapeutic
agents
inhibitors
are
currently
being
developed.
In
this
review,
we
first
provide
a
summary
multiple
biological
functions
oncoprotein
in
cancer
treatment,
highlighting
equilibrium
points
MYC/MAX,
MIZ1/MYC/MAX,
MAD
(MNT)/MAX
complexes
further
potential
treatment
could
used
restrain
oncogene
expression
its
tumorigenesis.
We
also
discuss
multifunctional
capacity
various
cellular
processes,
influences
on
immune
response,
metabolism,
cell
cycle,
apoptosis,
autophagy,
pyroptosis,
metastasis,
angiogenesis,
multidrug
resistance,
intestinal
flora.
Moreover,
summarize
therapy
patent
landscape
emphasize
as
druggable
target,
using
herbal
medicine
modulators.
Finally,
describe
pending
challenges
future
perspectives
biomedical
research,
involving
development
approaches
modulate
or
targeted
genes.
Patients
with
cancers
driven
by
signaling
may
benefit
from
therapies
targeting
these
pathways,
which
delay
cancerous
growth
recover
antitumor
responses.
Cancers,
Journal Year:
2025,
Volume and Issue:
17(2), P. 248 - 248
Published: Jan. 14, 2025
The
epidermal
growth
factor
receptor
(EGFR)
regulates
gene
expression
through
two
primary
mechanisms:
as
a
in
the
nucleus,
where
it
translocates
upon
binding
its
ligand,
or
via
intrinsic
tyrosine
kinase
activity
cytosol,
modulates
key
signaling
pathways
such
RAS/MYC,
PI3K,
PLCγ,
and
STAT3.
During
tumorigenesis,
these
become
deregulated,
leading
to
uncontrolled
proliferation,
enhanced
migratory
metastatic
capabilities,
evasion
of
programmed
cell
death,
resistance
chemotherapy
radiotherapy.
RAS
MYC
oncogenes
are
pivotal
driving
processes
apoptosis,
replicative
immortality,
cellular
invasion
metastasis,
metabolic
reprogramming.
These
subject
regulation
by
range
epigenetic
post-transcriptional
modifications.
This
review
focuses
on
deregulation
EGFR,
RAS,
caused
(epi)genetic
alterations
post-translational
It
also
explores
therapeutic
potential
targeting
regulatory
proteins,
emphasizing
importance
phenotyping
neoplastic
tissues
inform
treatment
cancer.
Transcription,
Journal Year:
2025,
Volume and Issue:
unknown, P. 1 - 19
Published: Jan. 29, 2025
Protein
engineering
has
emerged
as
a
powerful
approach
toward
the
development
of
novel
therapeutics
targeting
MYC/MAX/E-box
network,
an
active
driver
>70%
cancers.
The
MYC/MAX
heterodimer
regulates
numerous
genes
in
our
cells
by
binding
Enhancer
box
(E-box)
DNA
site
and
activating
transcription
downstream
genes.
Traditional
small
molecules
that
inhibit
MYC
face
significant
limitations
include
toxic
effects,
drug
delivery
challenges,
resistance.
Recent
advances
protein
offer
promising
alternatives
creating
protein-based
drugs
directly
disrupt
dimerization
interface
and/or
MYC/MAX's
to
specific
targets.
Designed
proteins
like
Omomyc,
DuoMyc,
ME47,
MEF,
Mad
activity
through
dimerization,
sequestration,
DNA-binding
mechanisms.
Compared
molecules,
these
engineered
can
superior
specificity
efficacy
provide
potential
pathway
for
overcoming
traditional
cancer
therapies.
success
highlights
importance
developing
treatments.