Bergamo Alberta, Masi Alessia, Dyson Paul J, Sava Gianni
Callerio Foundation Onlus, 34127 Trieste, Italy.
Int J Oncol. 2008 Dec;33(6):1281-9.
The modulation of the metastatic progression of breast cancer has been evaluated in vitro and in vivo with RAPTA-T, [Ru(eta6-toluene)Cl2(PTA)], an organometallic ruthenium compound. In vitro RAPTA-T inhibits some steps of the metastatic process such as the detachment from the primary tumour, the migration/invasion and the re-adhesion to a new growth substrate. All these effects are boosted when cells grow on components of the extra cellular matrix such as collagen IV and fibronectin and minimized on the non-specific substrate poly-L-lysine and are more pronounced when experiments are performed with the highly invasive MDA-MB-231 cells than with the non-invasive MCF-7 or the non- tumourigenic HBL-100. In vivo RAPTA-T selectively reduces the growth of lung metastases, an effect that might be explained by the in vitro activity. The effect on tests requiring the interaction of the tumour cells with extra cellular matrix components, might suggest an interaction with cell surface molecules in the activity of this ruthenium compound.
已使用有机金属钌化合物RAPTA-T,即[Ru(η6-甲苯)Cl2(PTA)],在体外和体内评估了其对乳腺癌转移进程的调节作用。在体外,RAPTA-T抑制转移过程的某些步骤,如从原发性肿瘤脱离、迁移/侵袭以及重新黏附到新的生长底物上。当细胞在细胞外基质成分(如IV型胶原和纤连蛋白)上生长时,所有这些作用都会增强,而在非特异性底物聚-L-赖氨酸上则会减弱,并且在用高侵袭性的MDA-MB-231细胞进行实验时比用非侵袭性的MCF-7或非致瘤性的HBL-100细胞进行实验时更明显。在体内,RAPTA-T选择性地减少肺转移瘤的生长,这种作用可能由其体外活性来解释。对需要肿瘤细胞与细胞外基质成分相互作用的试验产生的影响,可能表明该钌化合物的活性与细胞表面分子存在相互作用。