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Originally published In Press as doi:10.1074/jbc.M904591199 on May 23, 2000

J. Biol. Chem., Vol. 275, Issue 32, 24767-24775, August 11, 2000
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c-Jun N-terminal Kinase Is Essential for Growth of Human T98G Glioblastoma Cells*

Olga PotapovaDagger , Myriam GorospeDagger , Frédéric Bost§, Nicholas M. Dean, William A. Gaarde, Dan Mercola§, and Nikki J. HolbrookDagger ||

From the Dagger  Cell Stress and Aging Section, Laboratory of Biological Chemistry, Gerontology Research Center, NIA, National Institutes of Health, Baltimore, Maryland 21224, § Sidney Kimmel Cancer Center, San Diego, California 91212, and  Isis Pharmaceuticals Inc., Carlsbad, California 92008

The c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) pathway is activated by numerous cellular stresses. Although it has been implicated in mediating apoptosis and growth factor signaling, its role in regulating cell growth is not yet clear. Here, the influence of JNK on basal (unstimulated) growth of human tumor glioblastoma T98G cells was investigated using highly specific JNK antisense oligonucleotides to inhibit JNK expression. Transient depletion of either JNK1 or JNK2 suppressed cell growth associated with an inhibition of DNA synthesis and cell cycle arrest in S phase. The growth-inhibitory potency of JNK2 antisense (JNK2 IC50 = 0.14 µM) was greater than that of JNK1 antisense (JNK1 IC50 = 0.37 µM), suggesting that JNK2 plays a dominant role in regulating growth of T98G cells. Indeed, JNK2 antisense-treated populations exhibited greater inhibition of DNA synthesis and accumulation of S-phase cells than did the JNK1 antisense-treated cultures, with a significant proportion of these cells detaching from the tissue culture plate. JNK2 (but not JNK1) antisense-treated cultures exhibited marked elevation in the expression of the cyclin-dependent kinase inhibitor p21cip1/waf1 accompanied by inhibition of Cdk2/Cdc2 kinase activities. Taken together, these results indicate that JNK is required for growth of T98G cells in nonstress conditions and that p21cip1/waf1 may contribute to the sustained growth arrest of JNK2-depleted T98G cultures.

* This work was supported in part by United States Public Health Service Grants NCI CA63783 and NCI CA76173 (to D. A. M.), California Breast Cancer Research Program Grant 8CB0246 (to D. A. M.), la Ligue Nationale Contre le Cancer (to F. B.), le Conseil Régional de Haute Normandie (to F. B.), the American Cancer Society, the Ray and Estelle Sephar Fellowship (to F. B.), and the fellowship program of the Sidney Kimmel Cancer Center.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

|| To whom correspondence should be addressed: Cell Stress and Aging Section, Laboratory of Biological Chemistry, Gerontology Research Center, National Institute on Aging, 5600 Nathan Shock Dr., Box 12, Baltimore, MD 21224. Tel.: 410-558-8446; Fax: 410-558-8386; E-mail: nikki_holbrook@nih.gov.

Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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