The
gut
microbiota
is
becoming
more
and
of
a
research
area
in
many
diseases,
including
cancer,
obesity,
diabetes,
brain
disease,
rheumatoid
arthritis,
cardiovascular
disease.
human
digestive
tract
contains
about
100
trillion
microorganisms.
Cancer
the
most
prevalent
malignancy
world.
likelihood
survival
can
be
increased
by
an
accurate,
early
diagnosis
necessary
medical
care.
Recent
studies
have
demonstrated
that
microbiome
has
impact
on
cancer.
Different
microbial
signatures
with
various
patterns
been
found
depending
stage
biological
subgroups.
In
shown
to
modulate
efficacy
anticancer
drugs.
changed
linked
resistance
immunological
checkpoint
inhibitors
(ICIs)
chemotherapy
treatments,
whereas
addition
certain
species
bacteria
restore
responsiveness
medications.
Various
evidence
suggested
potential
manipulation
increase
effectiveness
this
book
chapter,
we
focused
population
its
relationship
cancer
therapy
resistance,
particular
emphasis
serve
as
biomarker
for
Despite
important
results
from
preclinical
models
patient
clinical
data,
deeper
comprehension
interactions
between
aids
identification
novel
strategies
prevention,
stratification
patients
effective
treatment,
reduction
treatment
complications.
Cells,
Год журнала:
2024,
Номер
13(11), С. 958 - 958
Опубликована: Июнь 1, 2024
Autophagy
is
a
globally
conserved
cellular
activity
that
plays
critical
role
in
maintaining
homeostasis
through
the
breakdown
and
recycling
of
constituents.
In
recent
years,
there
has
been
much
emphasis
given
to
its
complex
cancer
stem
cells
(CSCs)
cell
treatment.
This
study
examines
molecular
processes
support
autophagy
how
it
regulated
context
CSCs
Although
dual
management
CSCs,
affecting
their
removal
as
well
maintenance,
intricate
interaction
between
several
signaling
channels
control
survival
death
part
mechanism
not
elucidated.
Given
have
development,
progression,
resistance
treatment
tumors,
imperative
comprehend
biological
activities.
are
important
for
biology
because
they
also
show
tissue
regeneration
model
helps
with
organoid
regeneration.
other
words,
manipulation
viable
therapeutic
approach
therapy.
Both
synthetic
natural
substances
target
pathways
demonstrated
promise
improving
cell-based
therapies
eliminating
CSCs.
Nevertheless,
difficulties
associated
limitations
CSC
regulation,
including
mechanisms
off-target
effects.
Thus,
regulation
offers
versatile
strategy
focusing
on
enhancing
results
Therefore,
understanding
interactions
would
be
essential
creating
treatments
work
both
regenerative
medicine
There
is
a
complex
and
strong
association
between
metabolic
reprogramming
the
phenomenon
of
drug
resistance
in
cancer.
Cancer
cell
modifications
crosstalk
with
cellular
noncellular
components
are
essential
to
support
their
growth
proliferation
anticancer
therapy
resistance.
The
chapter
explores
unintended
consequences
chemotherapy
interventions,
revealing
how
therapeutic
measures
can
induce
shifts
cancer
cells
that
inadvertently
contribute
emergence
chemoresistance.
navigates
through
complicated
interplay
key
genetic
players
mechanisms.
Finally,
proposes
innovative
strategies
manipulate
metabolism
as
promising
avenue
for
overcoming
This
comprehensive
examination
not
only
elucidates
link
but
also
suggests
potential
presenting
roadmap
future
research
evolving
landscape
treatment.
Autophagy
is
a
crucial
mechanism
that
maintains
the
balance
of
cellular
homeostasis
by
removing
faulty
or
unneeded
proteins
as
well
damaged
aged
organelles
in
cells.
triggered
formation
autophagosomes,
which
sequester
and
enclose
anomalous
constituents.
Subsequently,
autophagosomes
combine
with
lysosomes
to
efficiently
recycle
eliminate
degradative
cargo.
regulation
plays
dual
role
both
suppressing
promoting
cancer
many
types
malignancies
context-dependent
manner.
In
addition,
autophagy
regulates
characteristics
tumor
formation,
spread
cancer,
occurrence
stem
cells,
resistance
drugs
used
treatment.
regulators
are
employed
modify
for
purpose
anticancer
therapy.
However,
functions
hinder
their
effectiveness
this
therapy,
thereby
serving
primary
cause
treatment
failure.
The
chapter
provides
concise
overview
mechanisms
behind
its
correlation
carcinogenesis,
metastasis,
drugs.
Ultimately,
we
examine
potential
efficacy
addressing
prospective
therapeutic
approach
resistance.
Treating
cancer
has
so
many
hurdles,
and
drug
resistance
is
one
of
them.
Treatment
strategies
are
evolving
for
due
to
innate
acquired
capacity
in
The
mechanism
behind
the
constantly
response
new
treatment
an
outcome
or
adaptive
mutation
expression
cells.
In
a
broader
perspective,
can
be
governed
by
genetic,
epigenetic,
proteomic,
metabolic,
microenvironment
cues
that
ultimately
enable
selected
resistant
cells
survive
progress
under
unfavorable
conditions.
Although
been
widely
studied
progressively
leads
generation
targets
novel
anticancer
drugs
having
better
efficacy
than
previous
ones.
However,
high
variability
toward
existing
drugs,
strategic
options
with
need
explored
overcome
resistance.
Combination
therapy
used
alternative
success
rate
though
risk
amplified
side
effects
commonplace.
recent
groundbreaking
immune
combination
ways
revolutionized
greater
extent.
more
study
needed
done
at
metabolic
levels
identify
different
cancers
help
develop
therapies
effective
challenge
This
chapter
will
focus
on
challenges
opted
withstand
current
molecular
level.
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(20), С. 10874 - 10874
Опубликована: Окт. 10, 2024
Aberrant
signaling
through
damage-associated
molecular
patterns
(DAMPs)
has
been
linked
to
several
health
disorders,
attracting
considerable
research
interest
over
the
last
decade.
Adenosine
triphosphate
(ATP),
a
key
extracellular
DAMP,
activates
purinergic
receptor
P2X7,
which
acts
as
danger
sensor
in
immune
cells
and
is
implicated
distinct
biological
functions,
including
cell
death,
production
of
pro-inflammatory
cytokines,
defense
against
microorganisms.
In
addition
driving
inflammation
mediated
by
non-immune
cells,
persistent
release
endogenous
DAMPs,
ATP,
shown
result
epigenetic
modifications.
intestinal
diseases
such
inflammatory
bowel
disease
(IBD)
colorectal
cancer
(CRC),
consequent
amplification
response
resulting
reprogramming
may
impact
development
pathological
changes
associated
with
specific
phenotypes.
P2X7
overexpressed
gut
mucosa
patients
IBD,
whereas
blockade
prevents
chemically
induced
experimental
colitis.
Recent
data
suggest
role
for
determining
microbiota
composition.
Regulatory
mechanisms
downstream
receptor,
combined
signals
from
dysbiotic
microbiota,
trigger
intracellular
pathways
inflammasomes,
intensify
inflammation,
foster
colitis-associated
CRC
development.
Preliminary
studies
targeting
ATP-P2X7
pathway
have
favorable
therapeutic
effects
human
IBD
The
tumor
microenvironment
(TME)
is
an
ecosystem
that
surrounds
a
inside
the
body.
TME
contains
complex
and
dynamic
system
consists
of
various
cellular
noncellular
components
cross
talk
with
each
other
cells,
thus
supporting
progression.
intricate
interplay
between
cells
their
surrounding
has
emerged
as
pivotal
factor
influencing
development
drug
resistance
in
cancer
treatment.
This
book
chapter
explores
multifaceted
roles
plays
mediating
to
therapeutic
interventions
by
elucidating
interactions
immune
stromal
extracellular
matrix
components,
blood
vessels,
soluble
factors
within
TME.
It
unravels
complexity
mechanisms
through
comprehensive
exploration
key
signaling
pathways,
talk,
microenvironmental
factors,
highlights
contribution
TME-driven
adaptive
strategies
such
evasion,
epithelial-mesenchymal
transition,
angiogenesis
resistance.
also
specific
facets
including
role
cancer-associated
fibroblasts
(CAFs)
mesenchymal
stem
influence
(ECM)
fostering
active
participation
vascular
sustaining
are
dissected
this
chapter.
Further
digging
into
physiochemical
exchanges,
homotypic
heterotypic
interactions,
exosomes,
cytokines,
chemokines
critical
mediators
culminates
showcasing
innovative
targeting
overcome
resistance,
potentially
revolutionizing
treatment
paradigms.
In
essence,
provides
understanding
TME's
spanning
diverse
elements
while
illuminating
groundbreaking
approaches
mitigate
challenges
oncology.
Journal of Cellular Biochemistry,
Год журнала:
2023,
Номер
124(11), С. 1705 - 1719
Опубликована: Окт. 5, 2023
Abstract
Bone
marrow‐derived
mesenchymal
stem
cells
(BM‐MSCs)
are
considered
a
novel
regenerative
therapy
that
holds
much
potential.
This
study
aimed
to
examine
and
compare
the
ameliorative
effects
of
BM‐MSCs
compared
α‐tocopherol
(α‐Toc)
on
apoptosis,
autophagy,
β‐cell
function
in
rat
model
streptozotocin
(STZ)‐induced
diabetes
further
analyzed
implications
interrelations
entero‐insular
axis,
type
I
phosphoinositide
3‐kinase
(PI3K)/Akt
signaling.
Forty
adult
male
albino
rats
were
categorized
into
four
groups
(
n
=
10,
each):
control
group,
STZ‐induced
diabetic
group
(single
i.p.
injection
STZ
45
mg/kg),
treated
with
injection,
treatment
α‐Toc
p.o.
The
serum
glucose,
insulin,
nitric
oxide
(NO),
catalase
(CAT)
measured.
Histopathological
examination
pancreas,
expression
levels
CD44,
caspase‐3,
autophagy
markers,
P13K/Akt,
pancreas/duodenum
homeobox
protein
1,
pancreatic
tissue,
glucose‐dependent
insulinotropic
polypeptide
(GIP)
duodenum
detected
by
hematoxylin
eosin
staining,
immunofluorescence
labeling,
quantitative
real‐time
polymerase
chain
reaction.
showed
reduced
hyperglycemia,
nitrosative
stress
(NO,
CAT),
augmented
apoptosis
(caspase
3),
impaired
(p62/SQSTM1,
LC3),
downregulated
PI3K/Akt
pathway
increased
GIP
expression,
degeneration
islets.
Treatment
either
or
suppressed
stress,
recovered
upregulated
pathway,
subsequently
insulin
levels,
decreased
blood
partial
restoration
Based
our
findings,
cytoprotective
1‐induced
appeared
be
related
repaired
Moreover,
we
reported
their
reversing
intestinal
level.
effect
was
notably
superior
α‐Toc.
