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Epithelial-mesenchymal transition (EMT) has recently been recognised as a mechanism for cancer progression and malignant transformation. EMT by cancer cells does not follow an orderly program and is different from physiological and developmental EMT . EMT induced by growth factors and cytokines requires reprogramming of epithelial cells in order to reshape for locomotion and degradation of the extracellular matrix (ECM). Epithelial growth factor (EGF) has been described as a powerful mitogen for human ovarian surface epithelium (OSE) , where 90% of all ovarian carcinomas originate. The over-expression of EGF receptors (EGFRs) is common in human ovarian carcinoma-derived cell lines and tumours, thereby suggesting that the growth factor family plays a critical role in ovarian tumour aetiology and progression . EGF has been shown to induce EMT in epithelial cells and epithelial breast cancer cells.
Citation: Lim R, Lappas M, Ahmed N, Borregaard N, Quinn MA, et al. (2011) Effect of Silencing Neutrophil Gelatinase-Associated Lipocalin in Ovarian Cancer Cells on Epithelio-Mesenchymal Transition. J Mol Biomark Diagn 2:114
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