modulated AKT activation was found associated with the increase ofmigration.

Discussion: Our results indicated that miR-187 expression wasassociated with the progression of OSCC, and the strategy targetingmiR-187 expression could be advantageous for OSCC therapy.

doi:10.1016/j.oraloncology.2011.06.386

P144. MiR-134 expression is oncogenic for oral carcinomaS.-C. Lin *,a, W.-G. Shen a, C.-J. Liu a,b

a National Yang-Ming University, Taipei, Taiwan, ROCb MacKay Memorial Hospital, Taipei, Taiwan, ROC

Introduction: Oral squamous cell carcinoma (OSCC) is one of themost prevalent malignant diseases around the worldwide. Hence,understanding the mechanisms and pathogenesis of OSCC is impor-tant for improving the diagnosis and therapy against this disease.MicroRNAs (miRNAs; miRs) are small regulatory RNAs which can af-fect biological and pathological processes. Aberrant expression ofmiRNAs has been implicated in different types of cancers. Upregula-tion of miR-134 in OSCC was observed in a previous study. However,the clinical implications and functions of miR-134 in oral tumorigen-esis remain unclear.

Methods: Quantitative RT-PCR was used to analyze themiR-134expression in OSCC tissue pairs. The oncogenic phenotypes includingproliferation, migration and anchorage-independent colony forma-tion were assayed in cells with miR-134 expression or miR-134 block-age. The xenografic tumorigenecity was assayed on nude micemodel.

Results: miR-134 was found to be markedly upregulated incancerous tissues than in non-cancerous matched tissues in OSCCtissue pairs. Higher miR-134 was associated with the more ad-vanced tumor size and vascular invasion. Transfection of miR-134precursor transiently upregulated miR-134 expression in OSCC cells.It increased oncogenic potential of OSCC cells. Conversely, thein vitro oncogenic potential of OSCC cells was attenuated afterblocking of miR-134 expression. Stale SAS OSCC cell subclone withectopic miR-134 expression was established by lentiviral delivery.Ectopic miR-134 expression increased the tumorigenicity of SASsubclone.

Discussion: This identified for the first time that miR-134 is onco-genic to oral epithelium and its expression level could be validatedas a diagnostic marker of OSCC. An investigation towards regulationof miR-134 expression and miR-134 target gene will be beneficial totherapeutic intervention of OSCC.

doi:10.1016/j.oraloncology.2011.06.387

P145. Diversity of salivary gland tumors: Evidence with E-Cad-herin expression-an immunohistochemical studyS. Prabhu*, K. Rekha

SDM College of Dental Sciences, Dharwad, India

Objective: To assess any variation in the immunohistochemicalexpression of E-Cadherin in benign and malignant Salivary GlandTumors.

Mateterial and methods: A total of 60 cases of benign and malig-nant salivary gland tumors were evaluated immunohistochemicallyfor E-Cadherin expression. These included 10 cases of pleomorphicadenoma, 2 cases of canalicular adenoma, 2 cases of myoepitheli-

oma, 24 cases of adenoid cystic carcinoma, 12 cases of mucoepider-moid carcinoma, 9 cases of adenocarcinoma and 1 case of carcinomaex pleomorphic adenoma.

Results: Out of 60 cases, 48 (80%) showed positivity, of which be-nign tumors showed positive expression in 85.7% and malignant tu-mors in 78.3% cases.

Conclusion: The result showed variability and heterogeneousexpression for E-Cadherin in salivary gland tumors. However, statis-tically significant reduction in expression was evident in Mucoepi-dermoid Carcinoma and Adenocarcinoma, when compared toPleomorphic adenoma.

Note: Part of this study is published in Oral Oncology 2009;45(7):594–599.

doi:10.1016/j.oraloncology.2011.06.388

P146. Comparative analysis of the salivary proteome of oralsubmucous fibrosis – A preliminary studyM. Soumyaa, R.-M. Nirmal ⁄ a, K.-K. Suresh b, B. Shweta b,J.-K. Mahesh b

a Rajah Muthiah Dental College, Annamalai University, Indiab Proteomics Lab., Division of Organic Chemistry, National ChemicalLaboratories, India

Introduction: Oral submucous fibrosis (OSMF), a precancerouscondition most prevalent in the Southeast Asia, is a chronic debilitat-ing disease of the oral mucosa related to the extensive use of arecanut. Human saliva proteome analysis (HSP) involves comprehensiveidentification and quantification of proteins of the whole saliva andtheir post translational modifications which could help in under-standing the disease mechanism. Keeping in view the research gapsin understanding the pathogenesis of OSMF, the study approach in-cluded characterization of the entire protein profiles of saliva fromOSMF patients in an attempt to identify differentially expressed pro-teins which could unravel the molecular changes and biochemicalpathways that have diagnostic and therapeutic significance.

Method: The quantitative and qualitative differences in proteinprofiles were assessed by two dimensional gel electrophoresis fromthe saliva obtained from normal and OSMF patients after appropriatestandardization. Further, the differentially expressed proteins wereidentified by peptide mass fingerprinting (PMF) and tandem massspectrometry (MS/MS) by MALDI-Synapt-HDMS.

Result: The protein content of the saliva determined by Bradfordtechnique gave a value of 3.16 g/l for OSMF as compared to 4.7 g/l forcontrols. While characterizing proteins, 300 proteins were visualizedout of which 61 proteins were differentially expressed between nor-mal and OSMF saliva.

Discussion: Extraction of proteins from saliva of OSMF patientsyielded adequate levels of protein which can be used for proteomicanalysis. The 2D gel results of our work confirmed the report byLaura et al. (2007) that 150–200 g of whole saliva protein givesacceptable resolution and separation for subsequent characteriza-tion by PMS. Functional characterization of the 61 differentially ex-pressed proteins in OSMF involved diverse functional groups such asmetabolism, cell cycle regulation, immune response and proteaseinhibitors. Further research is encouraged to evaluate and validatethe role of individual proteins in the background of pathogenesisand precancerous nature of OSMF.

doi:10.1016/j.oraloncology.2011.06.389

Abstracts / Oral Oncology 47 (2011) S74–S156 S121