Oral squamous cell carcinoma invasion is associated with a laminin-5 matrix re-organization but independent of basement membrane and hemidesmosome formation. clues from an in vitro invasion model.

Abstract

The basement membrane (BM) molecule laminin-5 represents the major component of the anchoring filaments, the BM counterpart of the hemidesmosomes. Because laminin-5 is abundantly deposited adjacent to budding invasive carcinoma cells in vivo, a special invasion-promoting role is suspected. We present a 3D collagen type I gel invasion model for oral squamous cell carcinoma (OSCC) using the newly established OSCC cell lines PE/CA-PJ15, PE/CA-PJ34, and PE/CA-PJ41. The carcinoma cells on the surface of the collagen type I gel show an invasive growth exclusively in the presence of gel-inoculated (myo)fibroblasts yielded from nodular palmar fibromatosis or tumour stroma. The model is characterized by an immunohistochemical and ultrastrcutural failure of structural BM and hemidesmosome formation. In the model an invasion-associated modulation of the laminin-5 deposition (alpha3, clone BM165; gamma2, clone GB3) was demonstrated: in invasive areas a strong ribbon-like immunostaining in the tumor-gel interface. The results obtained from the invasion model suggest that the assumed invasion-promoting ability of the BM molecule laminin-5 is realized independent of a structural BM and hemidesmosome formation.