A Berndt, P Hyckel, A Könneker, D Katenkamp, H Kosmehl
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引用次数: 0
摘要
基底膜(BM)分子层粘连蛋白-5是锚定丝(BM对应的半膜)的主要成分。由于层粘连蛋白-5大量沉积在体内萌芽的浸润性癌细胞附近,因此被怀疑具有特殊的侵袭促进作用。我们利用新建立的口腔鳞状细胞癌细胞系 PE/CA-PJ15、PE/CA-PJ34 和 PE/CA-PJ41,建立了口腔鳞状细胞癌(OSCC)的 I 型胶原蛋白三维侵袭模型。Ⅰ型胶原凝胶表面的癌细胞只有在凝胶接种了结节性掌跖纤维瘤或肿瘤基质中的(肌)成纤维细胞的情况下才会出现侵袭性生长。该模型的特点是免疫组化和超微切口结构BM和半球形成失败。在该模型中,层粘连蛋白-5(α3,克隆 BM165;γ2,克隆 GB3)的沉积发生了与侵袭相关的改变:在侵袭区域,肿瘤-凝胶界面出现了强烈的带状免疫染色。从侵袭模型中获得的结果表明,假定的基质分子层粘连蛋白-5的侵袭促进能力是独立于结构基质和半膜小体的形成而实现的。
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.
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.