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Antisense oligodeoxynucleotide against human telomerase reverse transcriptase inhibits the proliferation of Eca-109 esophageal carcinoma cells.
[esophageal carcinoma]
Previous
studies
have
demonstrated
that
the
growth
of
tumor
cells
may
be
inhibited
by
antisense
oligonucleotides
(
ASODNs
)
targeted
against
human
telomerase
(
hTR
)
or
human
telomerase
reverse
transcriptase
(
hTERT
)
,
resulting
in
antitumor
activity
in
a
wide
variety
of
tumors
.
However
,
few
studies
have
investigated
the
effect
of
hTERT
gene
-targeted
ASODNs
on
telomerase
activity
and
cell
proliferation
in
human
esophageal
cancer
.
In
the
present
study
,
an
MTT
assay
was
used
to
determine
the
growth
inhibition
rate
of
Eca-
109
cells
treated
with
a
hTERT-targeted
phosphorothioate-
ASODN
(
PS-ASODN
)
.
An
inverted
microscope
was
used
to
observe
the
morphologic
changes
of
the
cells
following
treatment
with
5
μM
PS-ASODN
for
10
days
.
Telomerase
activity
was
detected
using
the
silver
staining
semi-quantitative
telomeric
repeat
amplification
protocol
(
TRAP
)
assay
.
Following
treatment
with
the
PS-ASODN
(
1
-
5
μmol
/
l
)
,
the
proliferation
of
the
Eca-
109
cells
was
inhibited
.
The
differences
in
inhibition
rate
between
the
PS-ASODN
and
blank
control
groups
were
statistically
significant
(
P
<
0
.
05
)
when
the
concentration
of
the
PS-ASODN
was
≥
2
μmol
/
l
,
whereas
no
statistically
significant
difference
was
identified
between
the
non-
specific
-
ASODN
and
blank
control
groups
.
The
inhibition
rate
increased
gradually
as
the
concentration
of
the
PS-ASODN
increased
and
with
time
,
suggesting
that
the
PS-ASODN
inhibited
the
growth
of
Eca-
109
cells
in
a
concentration-dependent
,
time-dependent
and
sequence-
specific
manner
.
The
growth
rate
of
the
cells
incubated
with
the
PS-ASODN
was
reduced
compared
with
that
of
the
control
cells
.
Cells
treated
with
the
PS-ASODN
became
round
,
suspended
and
reduced
in
size
.
The
PS-ASODN
was
also
found
to
inhibit
telomerase
activity
.
The
ability
of
the
PS-ASODN
to
inhibit
the
telomerase
activity
and
cell
proliferation
of
the
Eca-
109
cell
line
suggests
that
ASODNs
have
the
potential
to
be
novel
therapeutic
agents
for
the
treatment
of
esophageal
cancer
.
Diseases
Validation
Diseases presenting
"cancer"
symptom
achondroplasia
acute rheumatic fever
adrenal incidentaloma
alpha-thalassemia
benign recurrent intrahepatic cholestasis
cadasil
canavan disease
carcinoma of the gallbladder
cholangiocarcinoma
coats disease
congenital adrenal hyperplasia
congenital diaphragmatic hernia
cowden syndrome
cushing syndrome
cutaneous mastocytosis
dedifferentiated liposarcoma
dystrophic epidermolysis bullosa
epidermolysis bullosa simplex
erdheim-chester disease
erythropoietic protoporphyria
esophageal adenocarcinoma
esophageal carcinoma
esophageal squamous cell carcinoma
familial hypocalciuric hypercalcemia
familial mediterranean fever
gm1 gangliosidosis
heparin-induced thrombocytopenia
hereditary cerebral hemorrhage with amyloidosis
hirschsprung disease
hodgkin lymphoma, classical
inclusion body myositis
junctional epidermolysis bullosa
kabuki syndrome
kallmann syndrome
kindler syndrome
lamellar ichthyosis
liposarcoma
locked-in syndrome
lymphangioleiomyomatosis
monosomy 21
neuralgic amyotrophy
oculocutaneous albinism
oligodontia
oral submucous fibrosis
papillon-lefèvre syndrome
pendred syndrome
pleomorphic liposarcoma
primary effusion lymphoma
proteus syndrome
pyomyositis
pyruvate dehydrogenase deficiency
severe combined immunodeficiency
sneddon syndrome
systemic capillary leak syndrome
triple a syndrome
von hippel-lindau disease
waldenström macroglobulinemia
well-differentiated liposarcoma
werner syndrome
wiskott-aldrich syndrome
wolf-hirschhorn syndrome
x-linked adrenoleukodystrophy
This symptom has already been validated