Institute of Biophotonics, National Yang-Ming University, Taipei 11221, Taiwan.
Integr Biol (Camb). 2012 Feb;4(2):177-82. doi: 10.1039/c2ib00112h. Epub 2011 Dec 16.
We employ a microfluidic chip with three culture chambers to investigate the interactions among lung cancer cells, macrophages and myofibroblasts. By mixing the conditioned media of macrophages and myofibroblasts in this chip, we confirm that these two stromal cells have synergistic effects in accelerating the migration of cancer cells. However, as the myofibroblasts are pretreated with the conditioned medium of macrophages, the myofibroblasts' ability to enhance the migration of cancer cells is lowered. The tumour necrosis factor-α produced by macrophages reduces the expression of α-smooth muscle actin and the secretion of transforming growth factor-β1 in myofibroblasts. Once the tumour necrosis factor-α in the macrophage conditioned medium is neutralized, the macrophage medium-pretreated myofibroblasts can still accelerate the migration of cancer cells.
我们采用一种带有三个培养室的微流控芯片来研究肺癌细胞、巨噬细胞和肌成纤维细胞之间的相互作用。通过在该芯片中混合巨噬细胞和肌成纤维细胞的条件培养基,我们证实这两种基质细胞在加速癌细胞迁移方面具有协同作用。然而,由于肌成纤维细胞预先用巨噬细胞的条件培养基处理,因此肌成纤维细胞增强癌细胞迁移的能力降低。巨噬细胞产生的肿瘤坏死因子-α会降低肌成纤维细胞中α-平滑肌肌动蛋白的表达和转化生长因子-β1的分泌。一旦中和巨噬细胞条件培养基中的肿瘤坏死因子-α,经巨噬细胞培养基预处理的肌成纤维细胞仍能加速癌细胞的迁移。