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Blood, Vol. 95 No. 3 (February 1), 2000:
pp. 1039-1046
CD40 activation mediates p53-dependent cell cycle regulation
in human multiple myeloma cell lines
G. Teoh,
Y.-T. Tai,
M. Urashima,
S. Shirahama,
M. Matsuzaki,
D. Chauhan,
S. P. Treon,
N. Raje,
T. Hideshima,
Y. Shima, and
K. C. Anderson
From the Department of Adult Oncology, Dana-Farber Cancer Institute,
and the Department of Medicine, Harvard Medical School, Boston, MA; the
Department of Hematology, Singapore General Hospital, Republic of
Singapore; the Department of Pediatrics, Jikei University School of
Medicine, Tokyo; and the Center for Molecular Biology and Cytogenetics,
SRL, Inc, Tokyo, Japan.
It has been reported that the activation of multiple myeloma (MM)
cells by CD40 induces proliferation, growth arrest, and apoptosis. To
determine whether the biologic sequelae of CD40 activation in MM
cells depends on p53 function, we identified temperature-sensitive p53 mutations in the RPMI 8226 (tsp53E285K) and the HS Sultan (tsp53Y163H) MM cell lines. These cells were then
used as a model system of inducible wtp53-like function because wild-type-like p53 is induced at permissive (30°C) but not at restrictive (37°C) temperatures. Using p21-luciferase reporter assays, we confirmed that CD40 induces p53 transactivation in RPMI 8226 and HS Sultan cells cultured under permissive, but not restrictive,
conditions. Furthermore, CD40 activation of these MM cells under
permissive, but not restrictive, temperatures increased the expression
of p53 and p21 mRNA and protein. Importantly, CD40 activation induced
the proliferation of RPMI 8226 and HS Sultan cells at restrictive
temperatures and growth arrest and increased subG1 phase cells at
permissive temperatures. These data confirmed that CD40 activation
might have distinct biologic sequelae in MM cells, depending on their
p53 status.
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