Gene,
Journal Year:
2024,
Volume and Issue:
940, P. 149199 - 149199
Published: Dec. 27, 2024
Pre-existing
of
pulmonary
tuberculosis
(PTB)
poses
increased
lung
cancer
risk,
yet
the
molecular
mechanisms
remain
inadequately
understood.
This
study
sought
to
elucidate
potential
by
performing
comprehensive
analyses
differentially
expressed
genes
(DEGs)
in
peripheral
blood
mononuclear
cells
(PBMCs)
from
patients
with
PTB,
adenocarcinoma
(LUAD),
and
squamous
cell
carcinoma
(LUSC).
Microarray
assays
were
employed
analyze
DEGs
PBMCs
these
patients.
The
revealed
that,
compared
healthy
controls,
number
LncRNA
LUAD,
LUSC
801,
8,541,
7,796,
respectively.
Similarly,
mRNA
629,
4,865,
4,438,
These
transcripts
represent
significant
resources
for
identifying
diagnostic
differential
biomarkers
PTB.
Pathways
enriched
dysregulated
mRNAs
identified
through
GO
KEGG
pathway
analyses.
results
indicated
that
9
pathways
including
NOD-like
receptor
signaling
pathway,
cancer,
MAPK
co-enriched
across
groups,
providing
insights
into
which
PTB
may
increase
risk
development
progression.
Frontiers in Pharmacology,
Journal Year:
2024,
Volume and Issue:
15
Published: June 19, 2024
Hederagenin
(HG)
is
a
natural
pentacyclic
triterpenoid
that
can
be
isolated
from
various
medicinal
herbs.
By
modifying
the
structure
of
HG,
multiple
derivatives
with
superior
biological
activities
and
safety
profiles
have
been
designed
synthesized.
Accumulating
evidence
has
demonstrated
HG
its
display
pharmacological
against
cancers,
inflammatory
diseases,
infectious
metabolic
fibrotic
cerebrovascular
neurodegenerative
depression.
Previous
studies
confirmed
combat
cancer
by
exerting
cytotoxicity,
inhibiting
proliferation,
inducing
apoptosis,
modulating
autophagy,
reversing
chemotherapy
resistance
in
cells,
action
targets
involved
mainly
include
STAT3,
Aurora
B,
KIF7,
PI3K/AKT,
NF-κB,
Nrf2/ARE,
Drp1,
P-gp.
In
addition,
antagonize
inflammation
through
production
release
pro-inflammatory
cytokines
mediators
regulating
inflammation-related
pathways
targets,
such
as
MAPK,
JAK2/STAT3,
Keap1-Nrf2/HO-1,
LncRNA
A33/Axin2/β-catenin.
Moreover,
anti-pathogen,
anti-metabolic
disorder,
anti-fibrosis,
neuroprotection,
anti-depression
mechanisms
partially
elucidated.
The
diverse
properties
hold
significant
implications
for
future
research
development
new
drugs
derived
which
lead
to
improved
effectiveness
profiles.
Frontiers in Public Health,
Journal Year:
2025,
Volume and Issue:
13
Published: Feb. 6, 2025
The
adaptation
of
malignancy
to
therapy
presents
a
significant
challenge
in
cancer
treatment.
cell
cycle
plays
crucial
role
regulating
the
evolution
radio-
and
chemo-resistance
tumor
cells.
Cancer
stem
cells
(CSCs)
are
primary
source
resistance,
with
CD133
being
one
most
recognized
valuable
surface
markers
CSCs.
Evidence
increasingly
suggests
that
is
associated
resistance.
current
understanding
molecular
biological
function
limited,
leading
ongoing
debates
about
its
biology.
In
this
review,
we
explore
recent
research
emerging
trends
related
through
extensive
literature
content
analysis.
It
was
summarized
new
insights
into
relationships
signaling
pathways
resistant
aim
review
provide
foundational
how
these
their
interactions
impact
prognosis
inform
treatment
strategies.
ACS Infectious Diseases,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Feb. 26, 2025
One
of
the
primary
healthcare
problems
in
world
today
is
tuberculosis
(TB),
a
chronic
infectious
illness
brought
on
by
Mycobacterium
(M.
tuberculosis).
A
distinct
family
PE_PGRS
proteins,
encoded
M.
genome,
has
attracted
more
attention
because
their
involvement
immune
evasion
and
bacterial
pathogenicity.
Nevertheless,
specific
functions
mechanisms
action
for
majority
proteins
remain
largely
unexplored.
This
study
focuses
Rv2741
(PE_PGRS47)
gene,
which
exclusively
present
pathogenic
mycobacteria.
To
examine
function
host–pathogen
interactions,
we
created
recombinant
strains
smegmatis
smegmatis)
that
expressed
gene.
IL-1α
was
found
to
be
key
mediator
host
response
modulation
Rv2741.
downregulates
secretion
inhibits
MAPK
signaling
pathway,
particularly
p38
ERK1/2
pathways,
thereby
cooperatively
inhibiting
macrophage
autophagy
apoptosis.
Meanwhile,
decrease
directly
leads
changes
cytokine
pattern
reduction
nitric
oxide
(NO)
production.
multifaceted
regulatory
mechanism
ultimately
favors
survival
macrophages.
research
significantly
expands
our
understanding
function,
revealing
its
crucial
role
as
multifunctional
virulence
factor
tuberculosis.
International Journal of Molecular Sciences,
Journal Year:
2025,
Volume and Issue:
26(6), P. 2678 - 2678
Published: March 16, 2025
Despite
the
substantial
advances
in
cancer
therapies,
developing
safe
and
effective
treatment
methodologies
is
critical.
Natural
(plant-derived
compounds),
such
as
flavonoids,
might
be
crucial
a
methodology
without
toxicity
toward
healthy
tissues.
Prunin
flavonoid
with
potential
to
used
biomedical
applications.
has
yet
undergo
thorough
scientific
research,
its
precise
molecular
mechanisms
of
action
remain
largely
unexplored.
This
review
summarizes
therapeutic
prunin
for
first
time,
focusing
on
underlying
an
anticancer
compound.
gained
significant
attention
due
antioxidant,
anti-inflammatory,
effects.
aims
unlock
how
functions
at
level
exert
effects,
primarily
modulating
key
cellular
pathways.
Furthermore,
we
have
discussed
prunin’s
adjunctive
therapy
conventional
treatments,
highlighting
ability
strengthen
responses
while
decreasing
drug
resistance.
Moreover,
discussion
probes
into
innovative
delivery
methods,
particularly
nanoformulations,
that
address
bioavailability,
solubility,
stability
limitations
optimize
application.
By
providing
comprehensive
analysis
properties,
this
stimulate
further
exploration
using
agent,
thereby
progressing
development
targeted,
selective,
safe,
methods.
Research Square (Research Square),
Journal Year:
2025,
Volume and Issue:
unknown
Published: May 7, 2025
AbstractBackground
Chronic
inflammatory
lung
diseases,
including
chronic
obstructive
pulmonary
disease
(COPD),
are
characterized
by
structural
changes,
narrowing
of
the
small
airways,
and
destruction
parenchyma
caused
prolonged
inflammation.
Sustained
inflammation
mediated
macrophages
is
considered
to
play
a
critical
role
in
COPD
pathogenesis,
while
inductive
mechanisms
persistent
remain
unclear.
Methods
In
vitro,
RAW264.7
cells
were
treated
with
cigarette
smoke
extract
(CSE),
hydrogen
peroxide,
12-O-tetradecanoylphorbol-13-acetate.
Loss-of-function
assays
performed
using
MAPK
inhibitors
Itch-specific
knockdown.
In
vivo,
tissues
from
mice
exposed
whole-body
for
12
weeks,
as
well
clinical
samples
healthy
non-smokers,
smoker,
patients,
analyzed.
Results
We
revealed
that
thioredoxin-interacting
protein
(TXNIP)
participates
smoke-incited
NF-κB
activation
potentially
conducted
CSE
markedly
inhibits
TXNIP
expression
through
MAPKs-dependent
regulation,
accompanied
induction
iNOS/NO
COX-2.
The
decrease
was
also
detected
obtained
smoking
mice,
higher
occurred
simultaneously.
Additionally,
smoke-associated
oxidative
stress
initiated
proteasomal
degradation
followed
MAPKs-regulated
concurrently.
E3
ligase
Itch
elevated
mouse
lungs
peroxide-stimulated
cells,
whereas
specific
silencing
significantly
attenuated
activation.
Moreover,
distinctly
suppressed
tissues,
bronchoalveolar
lavage
fluid
peripheral
blood
mononuclear
patients
COPD.
Conclusion
Accordingly,
smoke-induced
causes
Itch-mediated
degradation,
leading
enabling
pathogenesis.