The candidate tumour suppressor p33ING1cooperates with p53 in cell growth control

Igor Garkavtsev, Irina A. Grigorian, Valeria S. Ossovskaya, Mikhail V. Chernov, Peter M. Chumakov and Andrei V. Gudkov ()
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Igor Garkavtsev: University of Calgary
Irina A. Grigorian: College of Medicine, University of Illinois at Chicago
Valeria S. Ossovskaya: Engelhardt Institute of Molecular Biology
Mikhail V. Chernov: Cleveland Clinic Foundation
Peter M. Chumakov: Engelhardt Institute of Molecular Biology
Andrei V. Gudkov: College of Medicine, University of Illinois at Chicago

Nature, 1998, vol. 391, issue 6664, 295-298

Abstract: Abstract The candidate tumour-suppressor gene ING1 has been identified by using the genetic suppressor element (GSE) methodology1. ING1 encodes a nuclear protein, p33ING1, overexpression of which inhibits growth of different cell lines. The properties of p33ING1suggest its involvement in the negative regulation of cell proliferation and in the control of cellular ageing, anchorage dependence and apoptosis1,2,3. These cellular functions depend largely on the activity of p53, a tumour-suppressor gene that determines the cellular response to various types of stress4. Here we report that the biological effects of ING1 and p53 are interrelated and require the activity of both genes: neither of the two genes can, on its own, cause growth inhibition when the other one is suppressed. Furthermore, activation of transcription from the p21/WAF1 promoter, a key mechanism of p53-mediated growth control, depends on the expression of ING1. A physical association between p33ING1and p53 proteins has been detected by immunoprecipitation. These results indicate that p33ING1is a component of the p53 signalling pathway that cooperates with p53 in the negative regulation of cell proliferation by modulating p53-dependent transcriptional activation.

Date: 1998
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DOI: 10.1038/34675

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