Journal of Cancer Research and Clinical Oncology,
Год журнала:
2024,
Номер
150(6)
Опубликована: Июнь 4, 2024
Abstract
Background
Butyrate
is
a
common
short-chain
fatty
acids
(SCFA),
and
it
has
been
demonstrated
to
regulate
the
development
of
breast
cancer
(BC),
while
underlying
mechanism
still
unreported.
Methods
Gas
chromatography
was
used
measure
amounts
SCFA
(acetate,
propionate,
butyrate)
in
feces.
Cell
viability
measured
by
CCK-8
assay.
The
wound
healing
assay
cell
migration,
transwell
invasion.
levels
protein
gene
were
determined
western
blot
RT-qPCR
assay,
respectively.
Results
lower
faecal
samples
from
BC
patients
compared
control
samples.
In
cellular
experiments,
butyrate
significantly
suppressed
viability,
migration
invasion
T47D
dose-dependent
manner.
animal
effectively
impeded
growth
tumors.
Toll
like
receptor
4
(TLR4)
highly
expressed
tumors
patients.
inhibited
expression
TLR4.
addition,
promoted
cuproptosis-related
genes
including
PDXK
(pyridoxal
kinase)
SLC25A28
(solute
carrier
family
25
member
28),
which
lowly
Importantly,
overexpression
TLR4
can
reverses
promotion
prevention
malignant
biological
behaviors
cells.
Conclusion
summary,
inhibits
facilitating
through
inhibition
Our
investigation
first
identified
connection
among
butyrate,
progression.
These
findings
may
provide
novel
target
for
treatment
BC.
Frontiers in Immunology,
Год журнала:
2024,
Номер
15
Опубликована: Март 15, 2024
Chimeric
antigen
receptor
(CAR)
-T
cell
therapy
has
achieved
tremendous
efficacy
in
the
treatment
of
hematologic
malignancies
and
represents
a
promising
regimen
for
cancer.
Despite
striking
response
patients
with
malignancies,
most
solid
tumors
treated
CAR-T
cells
have
low
rate
experience
major
adverse
effects,
which
indicates
need
biomarkers
that
can
predict
improve
clinical
outcomes
future
treatments.
Recently,
role
gut
microbiota
cancer
been
established,
growing
evidence
suggested
signatures
may
be
harnessed
to
personally
therapeutic
or
effects
optimizing
therapy.
In
this
review,
we
discuss
current
understanding
microbiota,
interplay
between
Above
all,
highlight
potential
strategies
challenges
harnessing
as
predictor
modifier
while
attenuating
toxicity.
Pharmaceuticals,
Год журнала:
2024,
Номер
17(5), С. 604 - 604
Опубликована: Май 8, 2024
The
involvement
of
the
gut
microbiota
in
anti-cancer
treatment
has
gained
increasing
attention.
Alterations
to
structure
and
function
bacteria
are
important
factors
development
cancer
as
well
efficacy
chemotherapy.
Recent
studies
have
confirmed
that
related
metabolites
influence
pharmacological
activity
chemotherapeutic
agents
through
interactions
with
immune
system.
This
review
aims
summarize
current
knowledge
how
malignant
tumor
chemotherapy
affect
microbiota,
regulates
host
response,
between
response
advances
strategies
for
efficiency
based
on
also
described.
Deciphering
complex
homeostasis
maintained
by
immunity
provides
a
solid
scientific
basis
bacterial
intervention
Cancer Research,
Год журнала:
2024,
Номер
84(5), С. 771 - 784
Опубликована: Янв. 8, 2024
Abstract
Colorectal
cancer
development
and
outcome
are
impacted
by
modifiable
risk
factors,
including
psychologic
stress.
The
gut
microbiota
has
also
been
shown
to
be
linked
factors.
Here,
we
found
a
marked
deteriorative
effect
of
chronic
stress
in
multiple
colorectal
models,
chemically
induced
(AOM/DSS),
genetically
engineered
(APCmin/+),
xenograft
tumor
mouse
models.
RNA
sequencing
data
from
colon
tissues
revealed
that
expression
stemness-related
genes
was
upregulated
the
stressed
group
activated
β-catenin
signaling,
which
further
confirmed
results
ex
vivo
organoid
analyses
as
well
vitro
cell
tumorigenicity
assays.
16S
rRNA
showed
disrupted
microbes,
antibiotic
treatment
fecal
transplantation
abolished
stimulatory
effects
on
progression.
Stressed
mice
displayed
significant
decrease
Lactobacillus
johnsonii
(L.
johnsonii)
abundance,
inversely
correlated
with
load.
Moreover,
protocatechuic
acid
(PCA)
identified
beneficial
metabolite
produced
L.
based
metabolome
LC/MS-MS
analysis.
Replenishment
or
PCA
blocked
stress-induced
progression
decreasing
expression.
Furthermore,
cGMP
pathway,
agonist
sildenafil
cancer.
Altogether,
these
identify
impacts
microbiome
support
Significance:
Chronic
stimulates
stemness
reducing
intestinal
abundance
its
enhance
forming
basis
for
potential
strategies
circumvent
aggressiveness.
See
related
commentary
McCollum
Shah,
p.
645
Journal of Translational Medicine,
Год журнала:
2024,
Номер
22(1)
Опубликована: Фев. 9, 2024
Abstract
Background
Overweight
is
known
to
be
an
important
risk
factor
for
colorectal
cancer
(CRC),
and
the
differences
in
intestinal
flora
among
CRC
patients
with
different
BMI
status
have
not
been
clearly
defined.
The
purpose
of
this
study
was
elucidate
abundance,
composition
biological
function
status.
Method
A
total
170
were
included
grouped
according
data
patients.
≥
24
kg/m
2
defined
as
overweight
group,
within
range
18.5–23.9
normal
weight
group.
Preoperative
stool
collection
both
groups
used
16S
rRNA
sequencing.
Total
RNA
extracted
from
17
tumor
tissue
samples
transcriptome
sequencing,
then
CIBERSORT
algorithm
convert
into
relative
content
matrix
22
kinds
immune
cells,
correlation
between
cells
immune-related
genes
under
states
analyzed.
Finally,
we
identified
BMI-related
differential
functional
pathways
analyzed
these
flora.
Result
There
no
significant
difference
α
diversity
β
analysis
group
Partial
least
square
discriminant
(PLS-DA)
could
divide
two
clusters
stratification.
33
by
linear
effect
size
(LEfSe),
which
Actinomyces,
Desulfovibrio
Bacteroides
significantly
enriched
ko00514:
Other
types
O-glycan
biosynthesis
are
a
positive
Clostridium
IV
Macrophages
M2
T
regulatory
(Tregs).
negative
Dendritic
activated
CD4
memory
activated.
Conclusions
richness
may
related
status,
enrichment
Desulphurvibrio
microenvironment
resides
has
landscapes,
suggesting
that
some
affect
process
regulating
cell
infiltration
gene
expression,
but
further
experiments
needed
confirm
this.
Journal of Cancer Research and Clinical Oncology,
Год журнала:
2024,
Номер
150(6)
Опубликована: Июнь 4, 2024
Abstract
Background
Butyrate
is
a
common
short-chain
fatty
acids
(SCFA),
and
it
has
been
demonstrated
to
regulate
the
development
of
breast
cancer
(BC),
while
underlying
mechanism
still
unreported.
Methods
Gas
chromatography
was
used
measure
amounts
SCFA
(acetate,
propionate,
butyrate)
in
feces.
Cell
viability
measured
by
CCK-8
assay.
The
wound
healing
assay
cell
migration,
transwell
invasion.
levels
protein
gene
were
determined
western
blot
RT-qPCR
assay,
respectively.
Results
lower
faecal
samples
from
BC
patients
compared
control
samples.
In
cellular
experiments,
butyrate
significantly
suppressed
viability,
migration
invasion
T47D
dose-dependent
manner.
animal
effectively
impeded
growth
tumors.
Toll
like
receptor
4
(TLR4)
highly
expressed
tumors
patients.
inhibited
expression
TLR4.
addition,
promoted
cuproptosis-related
genes
including
PDXK
(pyridoxal
kinase)
SLC25A28
(solute
carrier
family
25
member
28),
which
lowly
Importantly,
overexpression
TLR4
can
reverses
promotion
prevention
malignant
biological
behaviors
cells.
Conclusion
summary,
inhibits
facilitating
through
inhibition
Our
investigation
first
identified
connection
among
butyrate,
progression.
These
findings
may
provide
novel
target
for
treatment
BC.
