Kelly T, Yan Y, Osborne R L, Athota A B, Rozypal T L, Colclasure J C, Chu W S
Department of Pathology, Arkansas Cancer Research Center, University of Arkansas for Medical Sciences, Little Rock 72205-7199, USA.
Clin Exp Metastasis. 1998 Aug;16(6):501-12. doi: 10.1023/a:1006538200886.
Breast cancer cell lines vary in invasive behavior and one highly invasive cell line (MDA-MB-231) proteolytically degrades extracellular matrix with invadopodia (Thompson et al. 1992, J Cell Physiol, 150, 534-44; Chen et al 1994, Breast Cancer Res Treat, 31, 217-26). Invadopodial proteolysis of extracellular matrix is thought to be necessary for invasion; however, this has not been demonstrated directly. To obtain such evidence, normal (HBL-100) and malignant (MCF-7, MDA-MB-231) breast cells were evaluated for invadopodial proteolysis of extracellular matrix and invasive behavior. We report that invadopodial proteolysis of immobilized fibronectin is positively correlated with invasion of cells into type I collagen gels. Moreover, reducing the proteolytic activity of invadopodia with the metalloproteinase inhibitor, batimastat (BB-94), also decreases invasion indicating that breast cancer cell invasion is dependent upon proteolytically active invadopodia.
乳腺癌细胞系在侵袭行为上存在差异，一种高侵袭性细胞系（MDA-MB-231）通过侵袭伪足对细胞外基质进行蛋白水解降解（汤普森等人，1992年，《细胞生理学杂志》，150卷，534 - 544页；陈等人，1994年，《乳腺癌研究与治疗》，31卷，217 - 226页）。细胞外基质的侵袭伪足蛋白水解作用被认为是侵袭所必需的；然而，这尚未得到直接证实。为了获得此类证据，对正常（HBL - 100）和恶性（MCF - 7、MDA - MB - 231）乳腺细胞进行了细胞外基质的侵袭伪足蛋白水解作用及侵袭行为评估。我们报告，固定化纤连蛋白的侵袭伪足蛋白水解作用与细胞侵入I型胶原凝胶的侵袭能力呈正相关。此外，用金属蛋白酶抑制剂batimastat（BB - 94）降低侵袭伪足的蛋白水解活性，也会减少侵袭，这表明乳腺癌细胞的侵袭依赖于具有蛋白水解活性的侵袭伪足。
