目的：研究子宫内膜癌Ishikawa细胞中，雌激素通过钙离子通道及雌激素受体引发钙离子流继而影响细胞外信号调节激酶（extracellular signal-regulated kinases, ERK）活化通路的机制。方法：激光共聚焦实验检测雌激素作用下及加入雌激素受体的抑制剂ICI182780和钙通道阻滞剂nifedipine后胞浆内游离钙离子浓度的变化，Western-blotting方法检测同样条件下ERK通路的激活。结果：17β-雌二醇（17β-estrodiol, E2）和偶联牛血清白蛋白（bovine serum albumin, BSA）的17β-雌二醇（E2-BSA）在作用1 min后均可以引发瞬时的钙离子流，钙离子的浓度增高可以被雌激素受体的抑制剂ICI182780和钙通道阻滞剂nifedipine抑制。在Ishikawa细胞，E2可以快速激活ERK通路，加入雌激素受体抑制剂ICI182780后，E2作用5 min和30 min，ERK通路未被阻抑。加入钙离子通道阻滞剂nifedipine后，5 min时雌激素对ERK通路的激活未被阻抑，但30 min时nifedipine阻抑了ERK通路的激活。E2-BSA对ERK通路的活化也在作用30 min后被nifedipine阻抑。结论：雌激素可以通过钙离子通道快速激发钙离子流，进而影响ERK通路的活化。

Objective：To study the mechanism on extracellular signal-regulate kinases (ERK) signal transduction by calcium influx initiated by combination of  estrogen with calcium channels or estrogen receptor in endometrial cancer cell Ishikawa. Methods: Confocal test was used to determine the relative calcium mobilization by stimulation of estrodiol together with and without the inhibition of ICI182780 and nifedipine. Western-blotting was used to detect the protein expression of phosphorylated ERK1/2(P-ERK1/2) in the same condition. Results: The transient calcium flux initiated by 17β-estrodiol (E2) and a membrane-impermeable conjugate of estrogen and bovine serum albumin (E2-BSA), and the calcium mobilization could be inhibited by ICI182780 and nifedipine in 1 min. In Ishikawa cells, phosphorylation of ERK1/2 was stimulated by E2, and the phosphorylation could not be inhibited by E2 after the combination with ICI182780 in 5 min and in 30 min. The phosphorylation also could not be inhibited by E2-BSA after the combination with nifedipine in 5 min, but in 30 min the phosphorylation was decreased. The phosphorylation of ERK by E2-BSA was decreased by the combination with nifedipine in 30 min. Conclusion: The transient calcium flux initiated by estrogen has an effect on the activation of ERK signal pathway in endometrial carcinoma cells.