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目的:通过观察雌激素对子宫内膜癌KLE细胞中Notch信号通路的影响,探讨过表达雌激素核受体(estrogen receptor,ER)是否可以恢复雌激素对Notch信号通路的调控作用,继而调节细胞增殖活性。方法:MTT检测雌激素及Notch信号通路对细胞增殖活性的影响;RT-PCR及Western-blotting检测雌激素及Notch通路抑制剂DAPT对Notch表达的影响;质粒的抽提及转染使KLE细胞中的雌激素核受体ER过表达。结果:雌激素呈剂量依赖效应促进KLE细胞的增殖活性,其中以雌激素浓度为1.0×10~(-9)M时最明显(相对于对照组为1.25±0.026,P<0.05);抑制Notch信号通路的表达可以明显下调KLE细胞的增殖活性(0.76±0.02,P<0.05);在KLE细胞中,雌激素对Notch的表达没有明显的调控作用,但是将其雌激素核受体过表达后,雌激素可明显上调Notch的表达,并显著促进细胞的增殖活性(1.24±0.02,P<0.05)。结论:在ER阴性的子宫内膜癌细胞中过表达ER,可以恢复雌激素对Notch信号通路的调控,从而进一步的调控细胞增殖活性。
OBJECTIVE: To observe whether Estrogen receptor (ER) overexpression plays an important role in regulating Notch signaling pathway in endometrial carcinoma cell line KLE and whether estrogen receptor (ER) overexpression regulates the regulation of Notch signaling pathway by estrogen, Proliferative activity. Methods: The effects of estrogen and Notch signaling pathway on the proliferation of cells were detected by MTT assay. The effects of estrogen and Notch pathway inhibitor DAPT on Notch expression were detected by RT-PCR and Western-blotting. The plasmid extraction and transfection Of estrogen nuclear receptor ER overexpression. Results: Estrogen promoted the proliferation of KLE cells in a dose-dependent manner. The estrogen dose-dependently increased the proliferative activity of KLE cells at the concentration of 1.0 × 10 ~ (-9) M (1.25 ± 0.026, P <0.05) The expression of NF-κB in KLE cells was significantly down-regulated (0.76 ± 0.02, P <0.05). In KLE cells, estrogen had no obvious effect on the expression of Notch. However, after overexpression of estrogen, , Estrogen could obviously up-regulate the expression of Notch, and significantly promote the proliferation activity of cells (1.24 ± 0.02, P <0.05). Conclusion: Overexpression of ER in ER-negative endometrial cancer cells can restore estrogen regulation of Notch signaling pathway and further regulate cell proliferation.