Oral squamous cell carcinoma (CEO) constitutes approximately 90% of oral malignancies and it is defined as an invasive cancer of epithelial origin showing varying degrees of squamous differentiation. It can occur at all sites in the mouth. The floor of the mouth and tongue are affected in approximately 41% to 74% of cases. The ethiology of CEO is multifactorial with the participation of intrinsic and extrinsic factors.Histological aspects of the CEO include small nests of neoplastic epithelial cells that invade the underlying connective tissue often causing a reactive inflammatory response in the stroma.The identified molecular changes indicate mutations in P-53 gene and overexpression of EGF as some of the most common events in this malignancy. Many studies have focused on the genetic changes of the neoplastic parenchyma cells, however studies of the tumor microenvironment have been gaining importance.In this context, many studies have investigated the role of fibroblasts, vascularization, and lymphangiogenesis in tumor progression, particularly of the so-called cancer-associated fibroblasts (CAFS). The mioma model was developed to allow a more accurate reproduction of the tumor microenvironment, including the presence of CAFS.Among the proteins involved in the neoplastic characteristics of invasion and metastasis production the matrix metalloproteinases (MMPs). Recent data indicated that MMP13 has a key role in metastasis development.This study will investigate cell invasiveness of a squamous cell carcinoma lineage (CAL27), stimulated by EGF, using the mioma model. MMP13 expression will be studied by ELISA.
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