title: ORAOV1 is amplified in oral squamous cell carcinoma.
abstract: 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Departmento de Patologia Bucal, Faculdade de Odontologia, Universidade de São Paulo, São Paulo, Brazil.
authors.forename: Flávia Caló Aquino
authors.initials: FC
authors.lastname: Xavier
authors.forename: Camila Oliveira
authors.initials: CO
authors.lastname: Rodini
authors.forename: Katiúcia Batista Silva
authors.initials: KB
authors.lastname: Paiva
authors.forename: Maria Fernanda Souza Setúbal
authors.initials: MF
authors.lastname: Destro
authors.forename: Patricia
authors.initials: P
authors.lastname: Severino
authors.forename: Raquel A
authors.initials: RA
authors.lastname: Moyses
authors.forename: Eloiza H
authors.initials: EH
authors.lastname: Tajara
authors.forename: Fabio Daumas
authors.initials: FD
authors.lastname: Nunes
mesh_terms: D000328:Adult; D002294:Carcinoma, Squamous Cell / Q000235:genetics* / Q000473:pathology / Q000556:secondary; D016022:Case-Control Studies; D045744:Cell Line, Tumor; D002880:Chromosomes, Human, Pair 11 / Q000235:genetics; D056915:DNA Copy Number Variations / Q000235:genetics; D004273:DNA, Neoplasm / Q000235:genetics; D005260:Female; D005500:Follow-Up Studies; D005784:Gene Amplification / Q000235:genetics*; D015972:Gene Expression Regulation, Neoplastic / Q000235:genetics; D006801:Humans; D008207:Lymphatic Metastasis / Q000473:pathology; D008297:Male; D009062:Mouth Neoplasms / Q000235:genetics* / Q000473:pathology; D060787:Neoplasm Grading; D009361:Neoplasm Invasiveness; D009363:Neoplasm Proteins / Q000235:genetics*; D009364:Neoplasm Recurrence, Local / Q000473:pathology; D009367:Neoplasm Staging; D009857:Oncogenes / Q000235:genetics*; D011446:Prospective Studies; D012333:RNA, Messenger / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015996:Survival Rate
chemical_list: D004273:DNA, Neoplasm; C465628:LTO1 protein, human; D009363:Neoplasm Proteins; D012333:RNA, Messenger