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*
Institute of Molecular Medicine, Huntington Memorial Hospital, Pasadena, CA 91105; and
Department of Microbiology and Immunology, University of California, Los Angeles, School of Medicine, Los Angeles, CA 90095-1747
AIDS-associated Kaposi’s sarcoma (KS) cell, a key element for
development of KS lesions, proliferates in response to external
cytokines, such as oncostatin M, the soluble IL-6R-IL-6 complex,
TNF-
, and IL-1ß. In addition, the KS cell-produced basic
fibroblast growth factor (bFGF) was reported to function as an
autocrine growth factor. However, little is known of the exact roles of
these external growth factors and endogenous bFGF on proliferation of
KS cells, and underlying intracellular events have remained to be
defined. We obtained evidence that anti-bFGF Ab abolished growth of
KS cells by preventing S phase entry of the cell cycle, even in the
presence of the external growth factors. Blockade of the FGF action
profoundly inhibited cyclin E expression and cyclin-dependent kinase-2
(CDK2) activity, but not D-type cyclin expression and CDK4 activity.
Exogenously added acidic FGF (aFGF), which generated a rapid tyrosine
phosphorylation of FGFR1 and FGFR2 on KS cells, reversed the inhibitory
effects of anti-bFGF Ab. Thus, FGF actions are essential for cyclin
E-CDK2 activity and S phase entry. We also observed that the presence
of external growth factors markedly induced cyclin E-CDK2 activity and
S phase entrance, while the addition of aFGF or bFGF alone was
insufficient to induce these responses. All this evidence shows that
integration of the activities of external growth factors and endogenous
bFGF is required for full activation of cyclin E-CDK2 activity and KS
cell proliferation.
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