Colorectal
cancer
(CRC)
remains
an
alarming
global
health
concern
despite
advancements
in
treatment
modalities
over
recent
decades.
Among
the
various
factors
contributing
to
CRC,
this
review
emphasizes
critical
role
of
epigenetic
mechanisms
its
pathogenesis
and
progression.
This
also
describes
potential
natural
compounds
altering
landscape,
focused
mainly
on
DNA
methylation,
histone
modification,
non-coding
RNAs.
Publications
from
previous
five
years
were
searched
retrieved
using
well-known
search
engines
databases
like
PubMed,
Google
Scholar,
ScienceDirect.
Keywords
CRC/colorectal
cancer,
CAC/Colitis
associated
inflammasomes,
modulation,
genistein,
curcumin,
quercetin,
resveratrol,
anthocyanins,
sulforaphane,
epigallocatechin-3-gallate
used
combinations
during
search.
These
predominantly
affect
pathways
such
as
Wnt/β-catenin,
NF-κB,
PI3K/AKT
suppress
CRC
cell
proliferation
oxidative
stress
enhance
anti-inflammation
apoptosis.
However,
their
clinical
use
is
restricted
due
low
bioavailability.
multiple
methods
exist
overcome
challenges
this,
including
but
not
limited
structural
modifications,
nanoparticle
encapsulations,
bio-enhancers,
novel
advanced
delivery
systems.
improve
supportive
therapies
that
target
progression
epigenetically
with
fewer
side
effects.
Current
research
focuses
enhancing
targeting
control
while
minimizing
effects,
emphasizing
improved
specificity,
bioavailability,
efficacy
standalone
or
synergistic
therapies.
Frontiers in Immunology,
Год журнала:
2025,
Номер
15
Опубликована: Янв. 21, 2025
Emerging
evidence
indicates
a
correlation
between
inflammation
and
the
development
progression
of
cancer.
Among
various
inflammatory
signals,
interleukin-17
(IL-17)
family
cytokines
serve
as
critical
link
IL-17
is
highly
versatile
pro-inflammatory
cytokine
that
plays
pivotal
role
in
host
defense,
tissue
repair,
pathogenesis
diseases,
cancer
progression.
During
early
stages
tumorigenesis,
signaling
directly
promotes
proliferation
tumor
cells.
Conversely,
has
been
shown
to
exhibit
antitumor
immunity
several
models
grafted
subcutaneous
tumors.
Additionally,
dynamic
changes
microbiome
can
influence
secretion
IL-17,
thereby
affecting
development.
The
specific
contingent
upon
its
functional
classification,
spatiotemporal
characteristics,
stage
In
this
review,
we
introduce
fundamental
biology
expression
profile
receptors
cancer,
while
also
reviewing
discussing
recent
advancements
regarding
pleiotropic
effects
mechanisms
inflammation-related
cancers.
Furthermore,
supplement
our
discussion
with
insights
into
by
which
impacts
through
interactions
microbiota,
explore
implications
therapy.
This
comprehensive
analysis
aims
enhance
understanding
potential
treatment.
Cells,
Год журнала:
2025,
Номер
14(7), С. 488 - 488
Опубликована: Март 25, 2025
Inflammation
is
an
essential
component
of
the
immune
response
that
protects
host
against
pathogens
and
facilitates
tissue
repair.
Chronic
inflammation
a
critical
factor
in
cancer
development
progression.
It
affects
every
stage
tumor
development,
from
initiation
promotion
to
invasion
metastasis.
Tumors
often
create
inflammatory
microenvironment
induces
angiogenesis,
suppression,
malignant
growth.
Immune
cells
within
interact
actively
with
cells,
which
drives
progression
through
complex
molecular
mechanisms.
triggered
by
factors
such
as
infections,
obesity,
environmental
toxins
strongly
linked
increased
risk.
However,
acute
responses
can
sometimes
boost
antitumor
immunity;
thus,
presents
both
challenges
opportunities
for
therapeutic
intervention.
This
review
examines
how
contributes
biology,
emphasizing
its
dual
role
tumorigenesis
potential
target.
International Journal of Molecular Sciences,
Год журнала:
2025,
Номер
26(1), С. 413 - 413
Опубликована: Янв. 6, 2025
Chronic
gastrointestinal
disorders
such
as
inflammatory
bowel
diseases
(IBDs)
and
irritable
syndrome
(IBS)
impose
significant
health
burdens
globally.
IBDs,
encompassing
Crohn’s
disease
ulcerative
colitis,
are
multifactorial
characterized
by
chronic
inflammation
of
the
tract.
On
other
hand,
IBS
is
one
principal
tract
functional
abdominal
pain
altered
habits.
Although
precise
etiopathogenesis
these
remains
unclear,
mounting
evidence
suggests
that
non-coding
RNA
molecules
play
crucial
roles
in
regulating
gene
expression
associated
with
inflammation,
apoptosis,
oxidative
stress,
tissue
permeability,
thus
influencing
progression.
miRNAs
have
emerged
possible
reliable
biomarkers,
they
can
be
analyzed
biological
fluids
patients
at
a
low
cost.
This
review
explores
IBDs
IBS,
focusing
on
their
involvement
control
hallmarks.
By
an
extensive
literature
employing
bioinformatics
tools,
we
identified
frequently
studied
concerning
diseases.
Ultimately,
specific
could
proposed
diagnostic
biomarkers
for
IBS.
Their
ability
to
secreted
into
biofluids
makes
them
promising
candidates
non-invasive
tools.
Therefore,
understanding
molecular
mechanisms
through
ways
which
regulate
immune
responses
provide
new
insights
pathogenesis
open
avenues
miRNA-based
therapeutic
interventions.
Frontiers in Oncology,
Год журнала:
2025,
Номер
15
Опубликована: Март 17, 2025
Inflammation,
a
hallmark
of
cancer,
has
been
associated
with
tumor
progression,
transition
into
malignant
phenotype
and
efficacy
anticancer
treatments
in
cancer.
It
affects
all
stages
from
the
initiation
carcinogenesis
to
metastasis.
Chronic
inflammation
induces
immunosup-pression,
providing
an
environment
conducive
carcinogenesis,
whereas
acute
antitumor
immune
response,
leading
suppression.
Solid
tumors
have
inflammatory
microenvironment
(TME)
containing
cancer
cells,
stromal
soluble
molecules,
which
plays
key
role
progression
therapy
response.
Both
cells
TME
are
highly
plastic
constantly
change
their
phenotypic
functional
properties.
Cancer-associated
inflammation,
majority
consists
innate
important
cell
plasticity,
development
drug
resistance.
Today,
combined
used
advanced
technologies,
such
as
single-cell
RNA
sequencing
spatial
molecular
imaging
analysis,
pathways
linking
chronic
largely
elucidated.
In
this
review
article,
we
highlighted
cellular
mechanisms
involved
cancer-associated
its
effects
on
treatment
We
also
comprehensively
setting
GI
cancers.
In
many
tumors,
the
tumor
suppressor
TP53
is
not
mutated,
but
functionally
inactivated.
However,
mechanisms
underlying
p53
functional
inactivation
remain
poorly
understood.
SETD8
sole
enzyme
known
to
mono-methylate
on
lysine
382
(p53K382me1),
resulting
in
inhibition
of
its
pro-apoptotic
and
growth-arresting
functions.
We
analyzed
p53K382me1
expression
clinical
colorectal
cancer
(CRC)
inflammatory
bowel
disease
(IBD)
samples.
Histopathological
examinations,
RNA
sequencing,
ChIP
assay
preclinical
vivo
CRC
models,
were
used
assess
role
cells
immune
cell
infiltration.
By
integrating
bulk
RNAseq
scRNAseq
approaches
patients,
SETD8-mediated
regulation
resulted
most
significantly
enriched
pathway.
was
confined
stem
(CR-CSCs)
C1Q+
TPP1+
tumor-associated
macrophages
(TAMs)
patient
tissues,
with
high
levels
predicting
decreased
survival
probability.
TAMs
promote
CR-CSCs
through
IL-6
MCP-1
secretion
increased
CEBPD,
which
directly
binds
promoter
thus
enhancing
transcription.
The
direct
binding
C1Q
present
receptor
(C1QR)
mediates
cross-talk
between
two
compartments.
As
monotherapy,
genetic
pharmacological
(UNC0379)
affects
growth
metastasis
formation
mouse
avatars,
enhanced
effects
observed
when
combined
targeting.
These
findings
suggest
that
may
be
an
early
step
initiation,
especially
inflammation-induced
CRC,
could
serve
as
a
biomarker
therapeutic
target
adjuvant
setting
for
advanced
CRCs.
Journal of Cellular Biochemistry,
Год журнала:
2024,
Номер
126(1)
Опубликована: Сен. 20, 2024
ABSTRACT
Metastatic
colorectal
carcinoma
(mCRC)
is
one
of
the
prevalent
subtypes
human
cancers
and
caused
by
alterations
various
lifestyle
diet‐associated
factors.
β‐catenin,
GSK‐3β,
PI3K‐α,
AKT1,
NF‐κB
p50
are
known
to
be
critical
regulators
tumorigenesis
immunopathogenesis
mCRC.
Unfortunately,
current
drugs
have
limited
efficacy,
side
effects
can
lead
chemoresistance.
Therefore,
searching
for
a
nontoxic,
efficacious
anti‐mCRC
agent
crucial
utmost
interest.
The
present
study
demonstrates
identification
productive
nontoxic
through
five‐targets
(β‐catenin,
p50)‐based
three‐tier
(binding
affinity,
pharmacokinetics,
pharmacophore)
screening
strategy
involving
series
30
phytocompounds
having
background
anti‐inflammatory/anti‐mCRC
efficacy
alongside
5‐fluorouracil
(FU),
reference
drug.
Luteolin
(a
phyto‐flavonoid)
was
eventually
rendered
as
most
potent
safe
phytocompound.
This
inference
verified
three
rounds
validation.
Firstly,
luteolin
found
effective
against
different
mCRC
cell
lines
(HCT‐15,
HCT‐116,
DLD‐1,
HT‐29)
without
hampering
viability
non‐tumorigenic
ones
(RWPE‐1).
Secondly,
curtail
clonogenicity
CRC
cells,
finally,
it
also
disrupted
formation
colospheroids,
characteristic
metastasis.
While
studying
mechanistic
insights,
inhibit
β‐catenin
activity
key
regulator
mCRC)
direct
physical
interactions,
promoting
its
degradation
activating
GSK3‐β
ceasing
activation
inactivating
AKT1
PI3K‐α.
inhibited
activity,
which
could
useful
in
mitigating
mCRC‐associated
proinflammatory
milieu.
In
conclusion,
our
provides
evidence
on
recommends
further
studies
animal
models
determine
effectiveness
this
natural
compound
treating
future.
International Journal of Colorectal Disease,
Год журнала:
2024,
Номер
39(1)
Опубликована: Окт. 28, 2024
Chronic
inflammation
is
a
significant
driver
in
the
development
of
various
diseases,
including
cancer.
Colitis-associated
colorectal
cancer
(CA-CRC)
refers
to
increased
risk
individuals
with
chronic
inflammatory
bowel
diseases
(IBD)
such
as
ulcerative
colitis
and
Crohn's
disease.
This
narrative
review
examines
link
between
CA-CRC.
A
comprehensive
literature
search
was
conducted
using
PubMed,
Scopus,
Web
Science,
focusing
on
studies
published
2000
2024.
Studies
were
selected
based
relevance
role
CA-CRC,
specifically
targeting
molecular
pathways
clinical
implications.
Both
mechanistic
reviewed.
Sustained
colon
fosters
pro-tumorigenic
environment,
leading
initiation
progression
Prevention
strategies
must
focus
controlling
inflammation,
optimizing
IBD
management,
implementing
regular
screenings.
Emerging
therapies
key
immune
responses,
along
microbiome
modulation,
hold
promise
for
reducing
CA-CRC
risk.
Understanding
these
mechanisms
provides
path
toward
personalized
treatment
better
outcomes
patients
at
Clinical and Experimental Medicine,
Год журнала:
2024,
Номер
24(1)
Опубликована: Окт. 29, 2024
Colorectal
cancer
(CRC)
ranks
among
the
most
prevalent
malignant
tumors
worldwide,
with
a
multifactorial
etiology
encompassing
genetic,
environmental,
and
life-style
factors,
as
well
intestinal
microbiota
its
metabolome.
These
risk
factors
often
work
together
in
specific
groups
of
patients,
influencing
how
CRC
develops
progresses.
Importantly,
alterations
gut
act
critical
nexus
this
interplay,
significantly
affecting
susceptibility
to
CRC.
This
review
highlights
recent
insights
into
unmodifiable
modifiable
for
they
might
interact
Understanding
mechanisms
these
interactions
will
help
us
develop
targeted,
precision-medicine
strategies
that
can
adjust
composition
meet
individual
health
needs,
preventing
or
treating
more
effectively.