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Volume 2, Issue 2 (Suppl)
Dent Implants Dentures, an open access journal
ISSN: 2572-4835
Dental Medicine 2017
October 16-18, 2017
October 16-18, 2017 New York, USA
29
th
Annual World Congress on
Dental Medicine & Dentistry
Role of EGFR inhibitors in oral cancer cell migration
Aye Myat Thwe
University of Dundee, United Kingdom
E
pithelial to mesenchymal transition (EMT) is the process by which cells change shape from being tightly connected epithelial
cells to more motile mesenchymal cell. EMT has been reported to facilitate cell migration. Cell motility is an initial first step on
the road to metastasis. Epidermal growth factor receptor (EGFR) has been reported to be overexpressed in oral cancer and is often
related with poor prognosis. Epidermal growth factor (EGF) and transforming growth factor (TGFα) are ligands that bind to EGFR
and can affect many different cellular processes such as proliferation, migration, apoptosis etc. In this project, cell proliferation,
migration, morphology change and EMT makers of HSG, AZA1, HacaT and TYS are measured by cell counting, scratch assay,
photographic image capturing and immunofluorescence in related with addition of 1 ng/ml, 10 ng/ml, 50 ng/ml of EGF and TGFα
incubated at different time point. 10 ng/ml and 50 ng/ml concentration induce morphology change (EMT like phenotype with
finger like projection) and increase migration while there is not much difference in cell proliferation. Their morphological changes
are completely blocked by 1hour pre-treatment with 5µM Gefitinib (EGFR tyrosine kinase inhibitor), 5 µM Erlotinib (EGFR TK
inhibitor) and 25 µM PD (MAPK inhibitor) while there is no blockage of cell migration.
Biography
Aye Thwe graduated from Myanmar with a Bachelor of Dental Surgery in 2010. After practicing as a Dentist for 2 years, she came to UK to study at University of Dundee.
She received an MRes in Oral Cancer, and progressed into the PhD programme. She is now in the 3rd year of her PhD programme.
a.m.thwe@dundee.ac.ukAye Myat Thwe, Dent Implants Dentures 2017, 2:2 (Suppl)
DOI: 10.4172/2572-4835-C1-002