Center for Molecular Medicine, University of Connecticut Health Center, 263 Farmington Ave, Farmington, CT 06030, USA.
Matrix Biol. 2012 Jun;31(5):299-307. doi: 10.1016/j.matbio.2012.03.002. Epub 2012 Apr 16.
There is considerable interest in understanding prostate cancer metastasis to bone and the interaction of these cells with the bone microenvironment. Osteonectin/SPARC/BM-40 is a collagen binding matricellular protein that is enriched in bone. Its expression is increased in prostate cancer metastases, and it stimulates the migration of prostate carcinoma cells. However, the presence of osteonectin in cancer cells and the stroma may limit prostate tumor development and progression. To determine how bone matrix osteonectin affects the behavior of prostate cancer cells, we modeled prostate cancer cell-bone interactions using the human prostate cancer cell line PC-3, and mineralized matrices synthesized by wild type and osteonectin-null osteoblasts in vitro. We developed this in vitro system because the structural complexity of collagen matrices in vivo is not mimicked by reconstituted collagen scaffolds or by more complex substrates, like basement membrane extracts. Second harmonic generation imaging demonstrated that the wild type matrices had thick collagen fibers organized into longitudinal bundles, whereas osteonectin-null matrices had thinner fibers in random networks. Importantly, a mouse model of prostate cancer metastases to bone showed a collagen fiber phenotype similar to the wild type matrix synthesized in vitro. When PC-3 cells were grown on the wild type matrices, they displayed decreased cell proliferation, increased cell spreading, and decreased resistance to radiation-induced cell death, compared to cells grown on osteonectin-null matrix. Our data support the idea that osteonectin can suppress prostate cancer pathogenesis, expanding this concept to the microenvironment of skeletal metastases.
人们对了解前列腺癌向骨骼转移以及这些细胞与骨骼微环境的相互作用非常感兴趣。骨连接蛋白/SPARC/BM-40 是一种富含骨骼的胶原蛋白结合细胞外基质蛋白。它在前列腺癌转移中表达增加,并刺激前列腺癌细胞的迁移。然而,成骨细胞和基质中的骨连接蛋白的存在可能会限制前列腺肿瘤的发展和进展。为了确定骨基质中的骨连接蛋白如何影响前列腺癌细胞的行为,我们使用人前列腺癌细胞系 PC-3 以及体外培养的野生型和骨连接蛋白缺失型成骨细胞合成的矿化基质来模拟前列腺癌细胞与骨骼的相互作用。我们开发了这种体外系统,因为体内胶原基质的结构复杂性无法通过重构胶原支架或更复杂的基底膜提取物等底物来模拟。二次谐波产生成像表明,野生型基质具有组织成纵向束的厚胶原纤维,而骨连接蛋白缺失型基质具有随机网络中的较细纤维。重要的是,一种前列腺癌转移到骨骼的小鼠模型显示出与体外合成的野生型基质相似的胶原纤维表型。与在骨连接蛋白缺失型基质上生长的细胞相比,当 PC-3 细胞在野生型基质上生长时,其细胞增殖减少,细胞铺展增加,并且对辐射诱导的细胞死亡的抵抗力降低。我们的数据支持骨连接蛋白可以抑制前列腺癌发病机制的观点,将这一概念扩展到骨骼转移的微环境。