Agrez M V, Chua F K
Discipline of Surgical Science, Faculty of Medicine, University of Newcastle, New South Wales, Australia.
Br J Cancer. 1990 Oct;62(4):567-72. doi: 10.1038/bjc.1990.331.
The mechanism of bowel obstruction in colorectal cancer is likely to involve interactions between tumour cells, host fibroblasts and the extracellular matrix. The role of fibroblast-mediated matrix reorganisation in malignant structures of the large bowel was examined in an in vitro collagen matrix model in which tumour cells and fibroblasts were cultured under serum-free conditions. Colon cancer cells secreted a factor(s) which enhanced the ability of colon fibroblasts to contrast a collagen matrix without an associated mitogenic response by the fibroblasts. Within uncontracted collagen gels marked elongation of fibroblast cell processes was observed in the presence of the tumour-derived factor(s). We propose that matrix reorganisation by host fibroblasts in the wall of the human colon is responsible, at least in part, for malignant large bowel obstruction.
结直肠癌中肠梗阻的机制可能涉及肿瘤细胞、宿主成纤维细胞与细胞外基质之间的相互作用。在体外胶原基质模型中研究了成纤维细胞介导的基质重组在大肠恶性结构中的作用,该模型中肿瘤细胞和成纤维细胞在无血清条件下培养。结肠癌细胞分泌一种因子,该因子增强了结肠成纤维细胞收缩胶原基质的能力,而成纤维细胞无相关的促有丝分裂反应。在未收缩的胶原凝胶中,在肿瘤衍生因子存在的情况下,观察到成纤维细胞的细胞突起明显伸长。我们认为,人类结肠壁中宿主成纤维细胞进行的基质重组至少部分导致了恶性大肠梗阻。