早期传代（少于30代）和晚期传代（大于250代）的RL95-2人类子宫内膜腺鳞状癌细胞暴露于表皮生长因子（EGF）会产生密度和浓度依赖性效应。在低播种密度下，EGF（20 nM）抑制早期传代细胞的生长，而在高播种密度下，4.98 nM和20 nM浓度的EGF刺激了它们的生长。此外，无论种子密度如何，晚期传代细胞的生长都受到0.0166 nM EGF的刺激和4.98 nM和20 nM EGF的抑制。在低种子密度下，EGF（20 nM）引起了两代细胞的明显形态学改变。在低播种密度下，两代细胞的入侵抑制在Matrigel涂层滤器上明显。而在高播种密度下，EGF增强了侵袭性。在高播种密度下，EGF刺激了尿激酶型纤维蛋白原激活剂活性的增加，这可能增加了细胞降解细胞外基质的能力。此外，在EGF处理后，两代高种子密度细胞对Matrigel的粘附能力与侵袭性相关。

Exposure of RL95-2 human endometrial adenosquamous carcinoma cells of early passage (less than 30 passages) and late passage (greater than 250 passages) to epidermal growth factor (EGF) resulted in density- and concentration-dependent effects. At low seeding density, EGF (20 nM) inhibited the growth of early passage cells, whereas at high seeding density, 4.98 nM and 20 nM concentrations of EGF stimulated their growth. Furthermore, the growth of late passage cells was stimulated by 0.0166 nM EGF and inhibited by 4.98 nM and 20 nM EGF at both seeding densities. EGF (20 nM) caused marked morphological changes of both passages at the low seeding density. Inhibition of invasion of both passages through Matrigel-coated filters was seen at low seeding density, while at the high seeding density, EGF enhanced invasiveness. At high seeding density, EGF stimulated an increase in urokinase type plasminogen activator activity, which may have augmented the ability of cells to degrade the extracellular matrix. In addition, the ability of high seeding density cells of both passages to adhere to matrigel after EGF treatment correlated with invasiveness.