雌二醇对子宫内膜癌Ishikawa细胞MAPK通路的激活及对增殖的影响
DOI: 10.3971/j.issn.1000-8578.2016.03.009
Keywords: 子宫内膜癌,雌二醇,MAPK通路,Relationship between Expression of p57KIP2 and cyclin E Proteins and Clinicopathologic Features in Endometrial Adenocarcinoma Tissues,Expression of Lumican in Invasive and Metastatic Endometrial Carcinoma Tissues,Relative Factors of Pelvic Nodal Metastasis in Endometrial Carcinoma,Mechanism of 2-methoxyestradiol Reversing Multidrug Resistance of K562/AO2 Cells,Effect of High-dose Mifepristone on Cell Cycle and Apoptosis of Endometrial Carcinoma,InhibitionEffect ofArtesunate on IshikawaCellLine Invitro,Expression and Significance of claudin-4 and PTEN in Endometrial Carcinoma,Relationship between Expression of VEGF2D and MLD and Lymph Node Metastasis in En2 dometrial Carcinoma,Expressions of Chk1/2 and Plk1 Protein in Endometrial Carcinoma,Effect of Matrine on Signaling Transduction of MAPK and JAK-STAT in SMMC-7721 Cell Line,Cancer-testis Antigen Sperm Protein 17 Overexpressed in Endometrial and Cervical Carci- nomas,Inhibitory Effect of Antiprogestins Mifepristone on the Proliferation of Endometrial Carcinoma HHUA Cell Line in Vitro,Effect of Different Type of p16 Gene Expression on The Telomerase Activity in Endometrial Carcinoma
Abstract:
摘要 目的 探讨雌激素是否能激活MAPK信号转导通路，以及对子宫内膜癌细胞增殖能力的影响。方法 培养子宫内膜癌Ishikawa细胞，按药物干预分为3组：雌二醇（E2）组、U0126（MAPK激酶抑制剂）+E2组、对照组。采用荧光定量PCR技术检测各组MEK1/2、ERK1/2 mRNA表达的变化；Western blot法检测各组p-MEK1/2、p-ERK1/2蛋白的活化程度；流式细胞仪检测各组的细胞周期比例；细胞集落形成实验检测各组细胞的增殖能力；体外穿膜实验比较各组细胞的迁移能力。结果 E2组MEK1/2、ERK1/2 mRNA表达增加（P=0.025, P=0.002），U0126+E2组中，U0126能阻断E2诱导MEK1/2、ERK1/2 mRNA的表达上调（P=0.000, P=0.000）。E2组p-MEK1/2、p-ERK1/2蛋白活化水平升高（P=0.049, P=0.028)；U0126+E2组中，U0126能阻断E2诱导的p-MEK1/2、p-ERK1/2蛋白活化（P=0.018, P=0.003）。E2组G1期细胞比例显著低于对照组及U0126+E2组（P=0.017），集落形成率显著高于对照组及U0126+E2组（P=0.009），穿过微孔的细胞数显著多于对照组及U0126+E2组（P=0.000）。结论 雌二醇通过激活MAPK通路，促进子宫内膜癌的发展，MEK抑制剂能阻断并抑制这一作用
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