RESUMEN
Newly synthesized retinoic acid derivative-retinamide (RII) was employed as differentiation inducing agent. Cultured tumor cells of epithelial origin were exposed to 10-5mol/L RII for 5 passages. These cells included mouse fore stomach carcinoma (MFC, lung metastatic rate 85%), human nasopharyngeal carcinoma (CNE-2Z, 56%), and clonal variants from CNE-2Z, CNE2L2 (100%) and CNE2L4 (13%) . The results of serial observation were as follows. The growth, clone-forming ability, motility, invasiveness of these tumor cells were obviously inhibted. Their adhesion to fibronectin and laminin was increased. Morphological ultrastructure changes, mainly of surface structure, were also observed. These changes suggested that RII made metastatic cells less aggressive and showed a tendency toward differentiation. After exposured to RII, different changes of oncogene and antioncogene expression of these tumor cells were detected. For example, RE caused expression of nm23in MFC cells, but down regulated (decreased) its expression in CNE2L2 cells and similar changes of rasH, fos, nm23, Rb. Expression were observed for CNE-2Z cells and its clonal variants CNE2L2 CNE2ZL2. RII down regulated both these oncogene and antioncogenes in both CNE-2Z and CNE2L2, but up regulated all of them in CNE2L4. The results indicated that oncogene and antioncogene may play different roles in different tumor cells, the same factor (RII) may lead to different changes of gene-expression in different metastatic tumor cells. So the function of oncogene and antioncogene may be of relativity and may be influenced by multifactors. Our data were mostly from in vitro experiments. It could not be deduced completely to a level as a whole in vivo.