Our scientific work mainly deals with the question how cell-cell and cell-matrix interactions and their associated signaling networks change during the progression of oral squamous cell carcinoma. Despite modern therapeutic advances the mortality rate of patients suffering from OSCC is still about 50%. One reason for this the lack of specific tumor markers for premalignant and malignant OSCC stages. In our work we focus on calcium dependent adhesion molecules , cadherins, which are responsible for the maintainance of cell junctions and epithelial architecture. Additionally we investigate secreted Proteins which negatively influence the tumor microenvironment leading to migration and invasion or increased proliferation. Truncated forms of P-cadherin or the facit collagen XVI seem to play a major role during OSCC progression.
Another target molecule is collagen XVI and its truncated forms. Collagen XVI, a FACIT collagen, is associated with extracellular fibrillar structures and connects to cells via integrins influencing cell signaling. Proteolytic cleavage in a tumor microenvironment leads to sequestration of truncated forms displaying a funtional gain.
In our research we conduct experiments with 2D and 3D cell culture of OSCC cell lines and primary cells isolated from OSCC patients