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[Cancer Research 62, 2072-2076, April 1, 2002]
© 2002 American Association for Cancer Research

Molecular Biology and Genetics

Epigenetic Inactivation of 14-3-3 {sigma} in Oral Carcinoma

Association with p16INK4a Silencing and Human Papillomavirus Negativity1

Milena Gasco, Alexandra K. Bell, Victoria Heath, Alex Sullivan, Paul Smith, Louise Hiller, Isik Yulug, Gianmauro Numico, Marco Merlano, Paul J. Farrell, Mahvash Tavassoli, Barry Gusterson and Tim Crook2

UO Oncologia Medica, Azienda Ospedaliera S Croce e Carle, 12100 Cuneo, Italy [M. G., G. N., M. M.]; Ludwig Institute for Cancer Research, Imperial College of Science and Medicine, St. Mary’s Campus, Norfolk Place, London W2 1PG, United Kingdom [A. S., P. J. F., T. C.]; Institute of Cancer Genetics, Brunel University, Uxbridge UB8 4SP, United Kingdom [P. S.]; CRC Trials Unit, Institute for Cancer Studies, Edgbaston, Birmingham B15 2TT, United Kingdom [L. H.]; Department of Molecular Biology and Genetics, Bilkent University, 06533 Ankara, Turkey [I. Y.]; Cancer Gene Therapy Group, King’s College London, The Rayne Institute, London SE5 9NU [M. T.]; and University Department of Pathology, Western Infirmary, Glasgow G11 6NT, Scotland [A. K. B., V. H., B. G.]

In vitro studies have identified 14-3-3{sigma} as a regulator of senescence in human keratinocytes. To assess its contribution to squamous neoplasia, we have analyzed genetic and epigenetic changes in this gene in squamous cell carcinomas (SCCs) and dysplastic lesions of the oral cavity. No mutations were detected in the coding sequence of 14-3-3{sigma} in 20 oral carcinomas, and there was loss of heterozygosity in only 7 of 40 informative cases. In contrast to the absence of genetic change, aberrant methylation within 14-3-3{sigma} was detected in 32 of 92 squamous cell carcinomas and in 3 of 6 oral dysplasias and was associated with reduced or absent expression at both mRNA and protein levels. Methylation was not detected in matched, normal epithelial tissue controls. Carcinomas in which 14-3-3{sigma} was methylated were significantly more likely to lack DNA sequences from human papillomavirus and to have coincident methylation of p16INK4a than cases that expressed 14-3-3{sigma}. Methylation was detected in SCC, both wild-type and mutant for p53, but was more commonly detected in cancers with wild-type p53. These results implicate coincident epigenetic abrogation of function in both {sigma} and p16INK4a in a subset of SCCs of the oral cavity.




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