Chen Jian-Ying, Zhang Bo, Wang Guo-Bin, Chen Dao-da
Department of General Surgery, Union Hospital, Tongji Medical College, Huazhong Science and Technology University, Wuhan 430022, China.
Zhonghua Wai Ke Za Zhi. 2004 Nov 22;42(22):1363-6.
To discuss the relationship between estradiol and the mitogenic activated protein kinase signal transduction pathway and the expression of the MAPK in the MCF-7 breast cancer cell-line.
Epithelial growth factor (EGF) and different concentration of estradiol to induce the expression of phosphospecific ERK1/2 (pERK1/2) in MCF-7 cell line was used and the expression of pERK1/2 with western-blotting was detected. Then antiestrogen ICI 182780 and MAPK inhibitor PD98059 to inhibit the expression of pERK1/2 was used. The cell cycle of MCF-7 was detected by FACS.
EGF could significantly induce the expression of pERK1/2. Estradiol could also induce the expression of pERK1/2, but the intensity was less than the induction of EGF. The percentage of cells in the G(2)/M cell cycle after estradiol induction increased (18.38%) compared to the control group (10.52%) (P < 0.05).
MAPK is an important regulatory signal in breast cancer. Its measurement in breast cancer tissues provides information about the degree of activation of various growth factor pathways. This molecule may also provide a molecular target for compounds designed to block cell proliferation.
探讨雌二醇与丝裂原活化蛋白激酶信号转导通路之间的关系以及丝裂原活化蛋白激酶（MAPK）在MCF - 7乳腺癌细胞系中的表达。
使用上皮生长因子（EGF）和不同浓度的雌二醇诱导MCF - 7细胞系中磷酸化特异性细胞外信号调节激酶1/2（pERK1/2）的表达，并用蛋白质免疫印迹法检测pERK1/2的表达。然后使用抗雌激素ICI 182780和MAPK抑制剂PD98059抑制pERK1/2的表达。通过流式细胞术检测MCF - 7的细胞周期。
EGF可显著诱导pERK1/2的表达。雌二醇也可诱导pERK1/2的表达，但强度低于EGF诱导的强度。与对照组（10.52%）相比，雌二醇诱导后处于G(2)/M细胞周期的细胞百分比增加（18.38%）（P < 0.05）。
MAPK是乳腺癌中的一个重要调节信号。在乳腺癌组织中对其进行检测可提供有关各种生长因子通路激活程度的信息。该分子也可能为旨在阻断细胞增殖的化合物提供分子靶点。
