posterpresentation
Description

Title: 2148 - The Role of MECT1-MAML2 Fusion Protein in Mucoepidermoid Carcinoma

Authors:

Esra Amoura (Presenter)
Universtiy of Sheffiled

Keith Hunter, School of Clinical Dentistry, University of Sheffield
Colin Bingle, University of Sheffield
Lynne Bingle, School of Clinical Dentistry, University of Sheffield

Abstract:

Objectives:
Mucoepidermoid carcinoma (MEC) is the most common salivary gland cancer. A significant proportion of MEC cases (≥50%) have been associated with a unique and recurrent gene translocation which results in the production of the MECT1-MAML2 fusion protein. Although the presence of this fusion protein could play a crucial role in tumour development and growth, its molecular pathogenesis remains elusive. The aim of this study was to try to understand the role of the MECT1-MAML2 fusion protein in MEC, to investigate its effect on the expression of CREB and NOTCH target genes and its ability to transform cells.

Methods:
To further understand the biological basis of the fusion protein we have generated an epitope tagged MECT1-MAML2 expression clone by amplifying the fusion gene from MEC-expressing cell lines (NCIH292 and UM-HMC).
The MECT1-MAML2 expression clone was transfected into a lung carcinoma cell line and primary salivary gland cells, isolated from human explanted tissues, to study the down-stream effects of fusion protein expression.
A three-dimensional (3D) organoid model of salivary glands was developed to validate the monolayer cell culture results.

Results: Flag and Myc tagged mammalian expression constructs have been successfully generated and verified with overlapping sequences to indicate 100% identity to the subject.
Primary salivary gland cells were successfully transfected; however, greater transfection efficiency was achieved with the mucoepidermoid cell line.
A 3-D organoid model, including a folded duct-like cell structure, has been developed following 14 days in culture.

Conclusions: We now have a number of valuable tools which will allow us to fully elucidate the role of the MECT1-MAML2 fusion protein in MEC tumorigenesis.

Student Presenter

This abstract is based on research that was funded entirely or partially by an outside source:
The Minstry of Higher Education, Tripoli, Libya

Disclosure Statement:
The submitter must disclose the names of the organizations with which any author have a relationship, the nature of the relationship, and the clinical or research area involved. The following is submitted: NONE

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