Cell cycle controlled interaction of nucleolin with the retinoblastoma protein and cancerous cell transformation

doi:10.1074/jbc.M513335200

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Papers In Press, published online ahead of print May 12, 2006
J. Biol. Chem, 10.1074/jbc.M513335200
Submitted on December 15, 2005
Revised on May 11, 2006
Accepted on May 12, 2006

Cell cycle controlled interaction of nucleolin with the retinoblastoma protein and cancerous cell transformation

Edgar Grinstein, Ying Shan, Leonid Karawajew, Peter J. F. Snijders, Chris J. L. M. Meijer, Hans-Dieter Royer, and Peter Wernet

Institute of Transplantation Diagnostics and Cellular Therapeutics, Heinrich Heine University Medical Center, Duesseldorf 40225

Corresponding Author: Edgar.Grinstein{at}itz.uni-duesseldorf.de

Retinoblastoma protein (Rb) is a multifunctional tumor suppressor, frequently inactivated in certain types of human cancer. Nucleolin is an abundant multifunctional phosphoprotein of proliferating and cancerous cells, recently identified as cell cycle regulated transcription activator, controlling expression of human papillomavirus type 18 (HPV18) oncogenes in cervical cancer. Here we find that nucleolin is associated with Rb in intact cells in G1 phase of the cell cycle, and the complex formation is mediated by the growth inhibitory domain of Rb. Association with Rb inhibits the DNA binding function of nucleolin and in consequence the interaction of nucleolin with the HPV18 enhancer, resulting in Rb-mediated repression of the HPV18 oncogenes. The intracellular distribution of nucleolin in epithelial cells is Rb-dependent, and an altered nucleolin localization in human cancerous tissues results from a loss of Rb. Our findings suggest that deregulated nucleolin activity due to a loss of Rb contributes to tumor development in malignant diseases, thus providing further insights into the molecular network for the Rb-mediated tumor suppression.

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