Insights from Studies with Oral Cleft Genes Suggest Associations between WNT-pathway Genes and Risk of Oral Cancer

Author:

Andrade Filho P.A.1,Letra A.2,Cramer A.2,Prasad J.L.3,Garlet G.P.4,Vieira A.R.2,Ferris R.L.1,Menezes R.5

Affiliation:

1. Department of Otolaryngology and Immunology, Hillman Cancer Institute, University of Pittsburgh

2. Department of Oral Biology, Center for Craniofacial and Dental Genetics, School of Dental Medicine, University of Pittsburgh, 619 Salk Hall, 3501 Terrace St., Pittsburgh, PA, 15261, USA

3. Department of Diagnostic Sciences, School of Dental Medicine, University of Pittsburgh

4. Department of Biological Sciences, School of Dentistry of Bauru, University of São Paulo, Brazil

5. Department of Oral Biology, Center for Craniofacial and Dental Genetics, School of Dental Medicine, University of Pittsburgh, 619 Salk Hall, 3501 Terrace St., Pittsburgh, PA, 15261, USA   rms59@pitt.edu

Abstract

Oral squamous cell carcinoma (OSCC) accounts for more than 90% of the malignant neoplasms that arise in the mucosa of the upper aerodigestive tract. Recent studies of cleft lip/palate have shown the association of genes involved in cancer. WNT pathway genes have been associated with several types of cancer and recently with cleft lip/palate. To investigate if genes associated with cleft lip/palate were also associated with oral cancer, we genotyped 188 individuals with OSCC and 225 control individuals for markers in AXIN2, AXIN1, GSK3β, WNT3A, WNT5A, WNT8A, WNT11, WNT3, and WNT9B. Statistical analysis was performed with PLINK 1.06 software to test for differences in allele frequencies of each polymorphism between cases and controls. We found association of SNPs in GSK3B (p = 0.0008) and WNT11 (p = 0.03) with OSCC. We also found overtransmission of GSK3B haplotypes in OSCC cases. Expression analyses showed up-regulation of WNT3A, GSK3B, and AXIN1 and down-regulation of WNT11 in OSCC in comparison with control tissues (P < 0.001). Additional studies should focus on the identification of potentially functional variants in these genes as contributors to human clefting and oral cancer.

Publisher

SAGE Publications

Subject

General Dentistry

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