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Targeting survival and cell trafficking in multiple myeloma and Waldenstrom macroglobulinemia using pan-class I PI3K inhibitor, buparlisib.
[waldenström macroglobulinemia]
The
phosphatidylinositol-
3
kinase
(
PI
3
K
)
pathway
is
activated
in
multiple
myeloma
(
MM
)
and
Waldenstrom
Macroglobulenima
(
WM
)
,
and
plays
a
crucial
role
in
tumor
progression
and
drug
resistance
.
In
this
study
,
we
characterized
the
role
of
pan-class
I
PI
3
K
inhibition
on
cell
trafficking
and
survival
of
MM
and
WM
cells
.
We
tested
the
effect
of
pan-class
I
PI
3
K
inhibition
by
siRNA
silencing
or
pharmacologic
inhibition
with
buparlisib
on
MM
cell
survival
,
apoptosis
and
cell
cycle
in
vitro
and
tumor
growth
and
mobilization
of
MM
cells
in
vivo
.
We
then
evaluated
buparlisib-dependent
mechanisms
of
induced
MM
cell
mobilization
.
Moreover
,
the
effect
of
buparlisib
on
cell
survival
,
apoptosis
,
and
adhesion
of
WM
cells
to
bone
marrow
stromal
cells
(
BMSCs
)
has
been
evaluated
.
We
showed
that
buparlisib
induced
toxicity
in
MM
cells
,
supported
by
induction
of
apoptosis
and
cell
cycle
arrest
.
Buparlisib
was
also
found
to
reduce
tumor
progression
in
vivo
.
Importantly
,
buparlisib
enhanced
MM
cell
mobilization
in
vivo
which
was
driven
by
decreased
adhesion
of
MM
cells
to
BMSCs
and
increased
chemotaxis
via
up-regulation
of
CXCR
4
expression
.
Similar
to
its
effects
on
MM
cells
,
buparlisib
also
induced
cell
survival
and
apoptosis
,
and
decreased
adhesion
in
WM
cells
.
These
data
highlight
the
critical
contribution
of
class
I
PI
3
K
signaling
to
the
regulation
of
survival
and
cell
dissemination
in
B-
cell
malignancies
.
Am
.
J
.
Hematol
.
89
:
1030
-
1036
,
2014
.
©
2014
Wiley
Periodicals
,
Inc
.
Diseases
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Diseases presenting
"also induced cell survival"
symptom
waldenström macroglobulinemia
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