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Cell Growth & Differentiation, Vol 2, Issue 10 487-493, Copyright © 1991 by American Association of Cancer Research

ARTICLES

Retinoic acid negatively regulates p34cdc2 expression during human neuroblastoma differentiation

C Gaetano, K Matsumoto and CJ Thiele
Molecular Genetics Section, National Cancer Institute, Bethesda, Maryland 20892.

p34cdc2 is a protein kinase that has an important role in controlling cell cycle progression and may regulate tumor suppressor gene activity. In this work, we show that the arrest of cell growth and induction of differentiation in a tumorigenic neuroblastoma cell line by retinoic acid (RA) is associated with a 75-fold decrease in the level of p34cdc2 protein. The RA induced decrease in p34cdc2 levels does not simply reflect the arrest of cell growth, because p34cdc2 levels are not reduced when neuroblastoma cells are growth arrested by nutrient deprivation. Furthermore, dephosphorylation of the tumor suppressor gene product RB, a substrate for the p34cdc2 kinase activity, is observed only when p34cdc2 levels are decreased in RA treated cells. These studies link regulation of cdc2 level, RB phosphorylation state, and induction of differentiation by RA and suggest that alterations in the cdc2 gene or in genes controlling its regulation contribute to tumorigenesis.


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C. Gaetano, T. Matsuo, and C. J. Thiele
Identification and Characterization of a Retinoic Acid-regulated Human Homologue of the unc-33-like Phosphoprotein Gene (hUlip) from Neuroblastoma Cells
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E. Lucarelli, D. R. Kaplan, and C. J. Thiele
Selective Regulation of TrkA and TrkB Receptors by Retinoic Acid and Interferon-[IMAGE] in Human Neuroblastoma Cell Lines
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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cell Growth & Differentiation
Copyright © 1991 by the American Association of Cancer Research.