Volume 41, Issue 1 pp. 54-60

ORAOV1 is amplified in oral squamous cell carcinoma

Flávia Caló Aquino Xavier

Flávia Caló Aquino Xavier

Departmento de Patologia Bucal, Faculdade de Odontologia, Universidade de São Paulo, São Paulo, SP, Brazil

Search for more papers by this author
Camila Oliveira Rodini

Camila Oliveira Rodini

Departmento de Patologia Bucal, Faculdade de Odontologia, Universidade de São Paulo, São Paulo, SP, Brazil

Search for more papers by this author
Katiúcia Batista Silva Paiva

Katiúcia Batista Silva Paiva

Departmento de Patologia Bucal, Faculdade de Odontologia, Universidade de São Paulo, São Paulo, SP, Brazil

Search for more papers by this author
Maria Fernanda Souza Setúbal Destro

Maria Fernanda Souza Setúbal Destro

Departmento de Patologia Bucal, Faculdade de Odontologia, Universidade de São Paulo, São Paulo, SP, Brazil

Search for more papers by this author
Patricia Severino

Patricia Severino

Centro de Pesquisa Experimental, Instituto Israelita de Ensino e Pesquisa Albert Einstein, São Paulo, SP, Brazil

Search for more papers by this author
Raquel A. Moyses

Raquel A. Moyses

Departamento de Cirurgia de Cabeça e Pescoço, Faculdade de Medicina, USP, São Paulo, SP, Brazil

Search for more papers by this author
Head and Neck Genome Project GENCAPO

Head and Neck Genome Project GENCAPO

Serviço de Cirurgia de Cabeça e Pescoço, Faculdade de Medicina de Ribeirão Preto, USP, São Paulo, SP, Brazil

Search for more papers by this author
Eloiza H. Tajara

Eloiza H. Tajara

Departamento de Biologia Molecular, Faculdade de Medicina de São José do Rio Preto, São José do Rio Preto, SP, Brazil

Departamento de Genética e Biologia Evolutiva, Instituto de Biociências da Universidade de São Paulo, São Paulo, SP, Brazil

Search for more papers by this author
Fabio Daumas Nunes

Fabio Daumas Nunes

Departmento de Patologia Bucal, Faculdade de Odontologia, Universidade de São Paulo, São Paulo, SP, Brazil

Search for more papers by this author
First published: 28 May 2011
Citations: 9
Fabio Daumas Nunes, Faculdade de Odontologia, Universidade de São Paulo, Av. Professor Lineu Prestes, 2227 - Cidade Universitária, São Paulo, SP, CEP 05508-000, Brazil. Tel: 55 11 3091 7902, Fax: 55 11 3091 7894, E-mail: [email protected]

The work was performed in Oral Pathology Department, School of Dentistry, University of São Paulo, Brazil.

Abstract

J Oral Pathol Med (2012) 41: 54–60

Background: Oral cancer overexpressed 1 (ORAOV1) was found as a candidate oncogene in the 11q13 chromosomal region, based on its amplification and overexpression in oral cancer cell lines. Because gene amplification often leads to increased levels of gene expression, we aimed to verify the relationship between ORAOV1 gene status and mRNA expression primarily in oral squamous cell carcinoma (OSCC) by quantitative assay, correlating with clinical and pathological characteristics in patients.

Methods: Levels of ORAOV1 amplification and expression were evaluated by qPCR and RT–qPCR in OSCC cell lines and in tumor and non-tumoral surgical margins from 33 patients with OSCC. All subjects were smokers and habitual alcohol drinkers, mostly men above 40 years of age and with a single primary tumor.

Results: ORAOV1 exhibited increased gene expression levels as well as higher copy number in three OSCC cell lines with 11q13 amplified chromosomal region when compared with the OSCC cell line without the amplification (one-way ANOVA, P < 0.05). Weak correlation between ORAOV1 mRNA levels and DNA copy number was seen in tumor samples (Spearman, P = 0.07). Although ORAOV1 was amplified in tumor (Wilcoxon, P < 0.01), high levels of transcripts in margin did not reveal differences in comparison with tumor (Wilcoxon, P = 0.85). Aggressiveness and survival rate did not demonstrate statistical difference for both events in OSCC.

Conclusion: The overexpression of ORAOV1 in non-tumoral margin samples can occur in the absence of amplification. The weak correlation between ORAOV1 amplification and expression in OSSC suggests that ORAOV1 expression can be regulated by mechanisms other than gene amplification.

The full text of this article hosted at iucr.org is unavailable due to technical difficulties.