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[Cancer Research 63, 2855-2863, June 1, 2003]
© 2003 American Association for Cancer Research

Molecular Biology and Genetics

Inhibition of BUB1 Results in Genomic Instability and Anchorage-independent Growth of Normal Human Fibroblasts1

Antonio Musio2, Cristina Montagna, Desirée Zambroni, Esterina Indino, Ottavia Barbieri, Lorenzo Citti, Anna Villa, Thomas Ried and Paolo Vezzoni

Istituto di Tecnologie Biomediche, Consiglio Nazionale delle Ricerche, Via Fratelli Cervi, 93, 20090 Segrate, Milan, Italy [A. M., D. Z., A. V., P. V.]; Genetics Branch, Center for Cancer Research, National Cancer Institute/NIH, Bethesda, Maryland 20892-0913 [C. M., T. R.]; Centro Ricerche Parco Scientifico "E. Menni," Ospedale Poliambulanza, 25100 Brescia, Italy [D. Z.]; Istituto Zooprofilattico Sperimentale delle Regioni Lazio e Toscana, Dipartimento di Firenze, 50010 Florence, Italy [E. I.]; Dipartimento di Oncologia Biologia e Genetica, Università di Genova, I.S.T., 16132 Genoa, Italy [O. B.]; and Istituto di Fisiologia Clinica, Consiglio Nazionale delle Ricerche, 56124 Pisa, Italy [L. C.]

The relative contribution of aneuploidy and gene mutations to human tumorigenesis is not yet known. Studies in mice have demonstrated that even single point mutations in oncogenes and tumor suppressor genes can dramatically increase tumor frequency. However, models to evaluate the definitive role of aneuploidy and genomic instability are not yet available. Human fibroblast cells have long been used as a tool for investigating proliferation, senescence, immortalization, and tumorigenesis, all processes that are strongly interrelated. We have now used antisense and ribozyme-mediated temporary inhibition of BUB1 to study the consequences of mitotic checkpoint failure on the development of aneuploidy. The analysis of cell colonies selected by soft agar growth showed evidence of chromosome instability and delayed senescence, without being tumorigenic in nude mice. Our data suggest that chromosomal instability and aneuploidy are early changes that precede tumorigenicity in the multistep process leading to neoplastic transformation.




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