Vossbeck H, Strahm B, Höfler P, Bauer G
Abteilung Virologie, Universität Freiburg, Germany.
Int J Cancer. 1995 Mar 29;61(1):92-7. doi: 10.1002/ijc.2910610116.
Treatment of NRK 536 fibroblasts with EGF and transforming growth factor type beta (TGF-beta) is known to lead to the reversible induction of the transformed phenotype in a large percentage of cells. Maintenance of the transformed state is dependent on the continuous presence of the cytokines. Here we show that treatment of these cells with TGF-beta alone leads to the formation of a small percentage of colonies, the majority of which stably retain the transformed phenotype after removal of the cytokine. Colony induction is dependent on the concentration of TGF-beta originally present. Stably transformed cells grow in soft agar without further addition of exogenous TGF-beta, and exhibit criss-cross morphology in monolayer culture and a diffuse actin pattern. Transformation of NRK 536 cells can be demonstrated only for individualized cells treated with TGF-beta in soft agar, as treatment in monolayer leads to the induction of apoptosis in newly transformed cells by neighboring normal cells. Transformation of NRK 536 fibroblasts by TGF-beta is not due to the induction of point mutations by TGF-beta.
已知用表皮生长因子（EGF）和β型转化生长因子（TGF-β）处理NRK 536成纤维细胞会导致很大比例的细胞可逆性诱导出转化表型。转化状态的维持取决于细胞因子的持续存在。在此我们表明，单独用TGF-β处理这些细胞会导致形成一小部分集落，其中大多数在去除细胞因子后稳定地保留转化表型。集落诱导取决于最初存在的TGF-β浓度。稳定转化的细胞在不进一步添加外源性TGF-β的情况下可在软琼脂中生长，并在单层培养中呈现交叉形态和弥漫性肌动蛋白模式。NRK 536细胞的转化仅在软琼脂中用TGF-β处理的单个细胞中得到证实，因为单层处理会导致新转化的细胞被邻近的正常细胞诱导凋亡。TGF-β对NRK 536成纤维细胞的转化并非由于TGF-β诱导点突变所致。
