Elvin P, Wong V, Evans C W
Exp Cell Biol. 1985;53(1):9-18. doi: 10.1159/000163290.
We have succeeded in selecting two variant strains of the Walker 256 carcinosarcoma which display markedly different adhesive properties. Both the high (W256A) and the low (W256S) adhesive variants respond chemotactically towards 10(-8) M f-met-leu-phe (FMLP) although there is a significant difference in their locomotory ability. Nevertheless, the fact that the essentially non-adherent W256S cells can migrate in vitro argues against any simple relationship between adhesion and locomotion. We suggest that traction is important in locomotion but that it need not arise only from direct adhesive interaction. We have also tested the invasive behaviour of the W256 variants using an in vitro model system in which disruption of a cellular barrier by the invasive cells can be recorded electrophysiologically. Although leucocytes can penetrate such a barrier they do so only under chemotactic stimulation, whereas W256 tumour cells of either variant strain will do so spontaneously. The tumour variants induce cell retraction within the barrier and this may lead ultimately to cell detachment and death. The holes which arise may then be colonized by tumour cells, and in this way the invasive process could be promoted. The molecular mechanisms by which tumour cells achieve destruction of the cellular barrier are not clear, but it is likely that a number of enzymes are involved.
我们成功筛选出了沃克256癌肉瘤的两种变异株，它们表现出明显不同的黏附特性。高黏附性变异株（W256A）和低黏附性变异株（W256S）对10(-8) M的甲酰甲硫氨酸-亮氨酸-苯丙氨酸（FMLP）均有趋化反应，尽管它们的运动能力存在显著差异。然而，基本不黏附的W256S细胞能够在体外迁移这一事实，反驳了黏附与运动之间存在任何简单关系的观点。我们认为牵引力在运动中很重要，但它不一定仅源于直接的黏附相互作用。我们还使用了一种体外模型系统来测试W256变异株的侵袭行为，在该系统中，侵袭细胞对细胞屏障的破坏可以通过电生理学方法记录下来。虽然白细胞只有在趋化刺激下才能穿透这样的屏障，但两种变异株的W256肿瘤细胞都会自发穿透。肿瘤变异株会诱导屏障内的细胞回缩，这最终可能导致细胞脱离和死亡。产生的孔洞随后可能会被肿瘤细胞占据，从而促进侵袭过程。肿瘤细胞破坏细胞屏障的分子机制尚不清楚，但可能涉及多种酶。
