Pippia P, Sciola L, Meloni M A, Barni S, Tilloca G
Boll Soc Ital Biol Sper. 1989 May;65(5):453-60.
In a study performed on transformed (SGS/3A) and normal syngeneic rat cells (FG/2) to identify the molecular mechanisms which regulate cell adhesion and contact inhibition in cell transformation, we investigated the effects of tumor promoters on cell to cell adhesion of rat fibroblasts. As tumor promoters we used 12-tetradecanoyl-phorbole-13-acetate (TPA) and the melittin, a polypeptide from bee venom, both substances capable of stimulating the neoplastic transformation. The intercellular adhesion assay consists in determining the percent of single cells labeled with 3H-L-leucine adhering to a confluent monolayer of unlabeled cells at different incubation times. The increase of cell-cell adhesion caused by TPA and melittin confirms what we have constantly observed in other experiments, i.e. that neoplastic cells SGS/3A always have a higher intercellular adhesion capacity than corresponding normal syngenic cells FG/2. Since one of the effects of the tumor promoters is also induction of a reversible alteration of the cytoskeleton, it is likely that their action on intercellular adhesion is regulated by a mechanism analogous to that proposed for explaining the increased intercellular adhesion observed after treatment with antimicrotubular compounds.
在一项针对转化的（SGS/3A）和同基因正常大鼠细胞（FG/2）进行的研究中，为了确定在细胞转化过程中调节细胞黏附和接触抑制的分子机制，我们研究了肿瘤启动子对大鼠成纤维细胞细胞间黏附的影响。作为肿瘤启动子，我们使用了12 - 十四烷酰佛波醇 - 13 - 乙酸酯（TPA）和蜂毒中的一种多肽蜂毒素，这两种物质都能够刺激肿瘤转化。细胞间黏附测定包括在不同孵育时间测定用³H - L - 亮氨酸标记的单细胞黏附到未标记细胞汇合单层上的百分比。TPA和蜂毒素引起的细胞间黏附增加证实了我们在其他实验中一直观察到的现象，即肿瘤细胞SGS/3A的细胞间黏附能力总是高于相应的同基因正常细胞FG/2。由于肿瘤启动子的作用之一也是诱导细胞骨架的可逆改变，它们对细胞间黏附的作用可能受一种类似于用于解释用抗微管化合物处理后观察到的细胞间黏附增加所提出的机制调节。
