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Vol. 55, Issue 2, 396-402, February 1999
Antisense Oligonucleotide
Department of Pharmacology (L.S., R.I.G.), and
Lombardi Cancer
Center (R.I.G.), Georgetown University, Washington, D.C.; and
ISIS
Pharmaceuticals, Inc., Carlsbad, California (N.M.D.)
Protein kinase C
(PKC) expression is related to tumor progression
in glioblastoma multiforme (GBM), the most common malignant brain tumor
in adults. To determine whether PKC regulates an anti-apoptotic
survival pathway in GBM, A172 GBM cells were treated with a
PKC-selective antisense oligonucleotide. PKC antisense oligonucleotide treatment was accompanied by reduction in PKC levels
and the induction of wild-type p53 and insulin-like growth factor-binding protein-3 (IGFBP3) 24-72 h after treatment, a period that coincided with the appearance of apoptotic cell death as detected
by DNA fragmentation. There were no significant changes in the levels
of Bcl-XL, Bax, and p21WAF1. Induction of p53
after PKC down-regulation was not associated with increased mRNA
expression, but increased IGFBP3 levels were accompanied by increased
mRNA levels. Recombinant human IGFBP3 induced an apoptotic effect that
was similar to the PKC antisense oligonucleotide, and its effect was
blocked by IGF-I. These results suggest that one mechanism by which
PKC produces its antiapoptotic activity in GBM cells is by
suppressing the p53-mediated activation of IGFBP3.
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