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Molecular adhesives in the spreading of epithelial ovarian carcinoma

Bogdan Waksmański1, Anita Olejek2

Affiliacja i adres do korespondencji
GIN ONKOL 2006, 4 (3), p. 193-201
Streszczenie

The spreading of epithelial ovarian carcinoma is associated with molecular mechanisms involving cell surface receptors, components of the basement membrane, intercellular adhesion molecules and cell-derived signals. A crucial role in cell adhesion and mobility is played by E-cadherin and catenin. The expression of the cadherin – catenin complex decreases with clinical progression of ovarian carcinoma. Simultaneously, this complex is re-expressed when neoplasia starts to spread across the peritoneum. A changing expression or malfunctioning of integrin receptors and their relationship with cells of the extracellular matrix (ECM) indicate a strong correlation with the progression of tumour or the potential of metastasis. Lysophosphatide acid mediates a laminin-induced cell migration in the local autocrine regulation. The first step in developing metastasis is the degradation of type IV collagen with the activity of metal proteinases and proangiogenic factors, which are observed to be highly expressed in ovarian carcinoma cells. An essential role in the migration of neoplastic cells that are negatively dependant on growth factors and integrin receptors is played by the kinase of focal adhesion contacts (FAK). An increased expression of this kinase involves a higher clinical progression of tumour, metastases to lymph nodes and the existence of distant metastases. A major prerequisite for metastasis to develop is a disorder of the cell adhesion mechanism, which consequently induces changes in the adhesion between cells and between cells and the extracellular matrix. This mechanism is of vital importance to the spreading of ovarian carcinoma within the abdominal cavity.

Słowa kluczowe
epithelial ovarian carcinoma, cell adhesion, FAK, cadherin