Rees A R, Adamson E D, Graham C F
Nature. 1979 Sep 27;281(5729):309-11. doi: 10.1038/281309a0.
Mouse teratocarcinoma stem cells (embryonal carcinoma, or EC cells) bind very small amounts of mouse epidermal growth factor (EGF) and the latter hormone seems to have no stimulatory effect on the growth of two cloned lines of EC cells. However, when EC cells are induced to differentiate into large flat endodern-like cells (END cells), EGF receptors increase in number reaching a plateau in 6 to 8 days. At 8 to 10 days after induction, END cells multiply very slowly, but when EGF is added (3 x 10(-10) M) to the medium, cell division is stimulated and a further change in morphology occurs. This letter describes the binding characteristics and numbers of the EGF receptors on EC and END cells and shows that exogenous retinoic acid increases the numbers of EGF receptors on END cells. We were unable to find endogenous competing factors produced by EC cells. Such factors could account for the lack of detectable binding of EGF on these cells. As EC cells differentiate to END cells, so the ability of the cells to form tumours is reduced. Since this change is accompanied by an increase in the number of EGF receptors there may be a relationship between these two events.
小鼠畸胎癌干细胞（胚胎癌，即EC细胞）仅结合极少量的小鼠表皮生长因子（EGF），而且后一种激素似乎对两株克隆的EC细胞系的生长没有刺激作用。然而，当EC细胞被诱导分化为大的扁平的内胚层样细胞（END细胞）时，EGF受体数量增加，并在6至8天达到稳定水平。诱导后8至10天，END细胞增殖非常缓慢，但当向培养基中加入EGF（3×10⁻¹⁰M）时，细胞分裂受到刺激，并且细胞形态发生进一步变化。本文描述了EC细胞和END细胞上EGF受体的结合特性及数量，并表明外源性视黄酸可增加END细胞上EGF受体的数量。我们未能找到EC细胞产生的内源性竞争因子。这类因子可能是导致在这些细胞上未检测到EGF结合的原因。随着EC细胞分化为END细胞，细胞形成肿瘤的能力降低。由于这种变化伴随着EGF受体数量的增加，这两个事件之间可能存在关联。
