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Kaposi's sarcoma-associated herpesvirus-encoded LANA can induce chromosomal instability through targeted degradation of the mitotic checkpoint kinase Bub1.
[primary effusion lymphoma]
Kaposi
's
sarcoma
-associated
herpesvirus
(
KSHV
)
has
a
significant
contributory
role
in
the
development
of
three
major
human
neoplastic
or
lymphoproliferative
diseases
:
Kaposi
's
sarcoma
(
KS
)
,
primary
effusion
lymphoma
(
PEL
)
,
and
multicentric
Castleman
's
disease
(
MCD
)
.
These
diseases
are
associated
with
chromosomal
instability
,
a
hallmark
of
human
cancer
.
The
latency-associated
nuclear
antigen
(
LANA
)
encoded
by
KSHV
plays
a
key
role
in
regulating
a
number
of
cellular
pathways
critical
for
oncogenesis
.
KSHV
LANA
alone
can
induce
the
development
of
B-
cell
hyperplasia
and
lymphoma
in
mice
expressing
LANA
.
LANA
also
induces
chromosomal
instability
,
thus
promoting
oncogenesis
.
However
,
the
precise
mechanism
underlying
LANA
-mediated
chromosomal
instability
remains
uncharted
.
Here
we
report
that
LANA
promoted
the
induction
of
chromosomal
instability
and
the
formation
of
micronuclei
and
multinucleation
through
its
interaction
with
one
of
the
critical
spindle
checkpoint
proteins
,
Bub
1
,
and
the
resulting
degradation
of
Bub
1
.
This
interaction
occurs
through
the
Knl
and
kinase
domains
of
Bub
1
,
identified
as
important
for
stability
and
degradation
.
These
results
suggest
that
LANA
can
dysregulate
Bub
1
activity
,
which
leads
to
aberrant
chromosome
replication
and
aneuploidy
,
thus
contributing
to
KSHV-mediated
oncogenesis
.
T
his
work
represents
the
first
set
of
results
identifying
a
novel
mechanism
by
which
LANA
,
a
latency-associated
antigen
encoded
by
KSHV
,
can
induce
the
degradation
of
Bub
1
,
a
spindle
checkpoint
protein
that
is
important
for
spindle
checkpoint
signaling
and
chromosome
segregation
.
The
downregulation
of
Bub
1
mediated
by
LANA
resulted
in
chromosomal
instability
,
a
hallmark
of
cancer
.
We
further
investigated
the
specific
domains
of
Bub
1
that
are
required
for
the
interaction
between
LANA
and
Bub
1
.
The
results
demonstrated
that
the
Knl
and
kinase
domains
of
Bub
1
are
required
for
the
interaction
between
LANA
and
Bub
1
.
In
addition
,
we
also
investigated
the
mechanism
by
which
LANA
promoted
Bub
1
degradation
.
Our
results
showed
that
LANA
interacted
physically
with
the
anaphase-promoting
complex
(
APC
/
C
)
,
thus
promoting
the
degradation
of
Bub
1
in
a
ubiquitin-dependent
process
.
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