本文選題：癌 + 非小細胞肺　； 參考：《重慶醫(yī)學》2017年05期

【摘要】：目的 研究G蛋白耦聯受體30(GPR30)在非小細胞肺癌(NSCLC)中的表達及其與臨床主要病理特征的關系,并分析GPR30和Ki-67表達的相關性,探討雌激素通過激活GPR30受體信號途徑調節(jié)NSCLC增殖的分子機制。方法 采用免疫組織化學方法檢測80例術后非小細胞肺癌組織樣本中GPR30和Ki-67的表達。加入17-β-雌二醇或G-1后,計數H1299細胞,流式細胞術檢測細胞周期分布,最后通過Western blot方法檢測G-1作用后ERK1/2的激活狀態(tài)以及cyclin D1和P16蛋白的表達。結果 GPR30更多表達在腺癌、低分化、Ⅲ期NSCLC腫瘤組織,差異有統計學意義(P0.05);GPR30表達和Ki-67呈中度相關性(r=0.502,P=0.000)。E2(或G-1)促進H1299細胞增殖,并且更多的細胞進入S期;加入G-1后,磷酸化ERK1/2以及cyclin D1表達增加,而p16蛋白表達減少,以上效應能被G-15或U0126預處理2h阻斷。結論 雌激素通過激活GPR30-EGFRMAPKs信號轉導途徑促進H1299增殖。阻斷GPR30信號途徑可能成為NSCLC治療的新靶點。
[Abstract]:Objective to study the expression of G-protein coupled receptor 30 (GPR30) in NSCLC and its relationship with the clinicopathological features, and to analyze the correlation between the expression of GPR30 and Ki-67.To explore the molecular mechanism of estrogen regulating NSCLC proliferation by activating GPR30 receptor signaling pathway.Methods Immunohistochemical method was used to detect the expression of GPR30 and Ki-67 in 80 cases of non-small cell lung cancer after operation.After adding 17- 尾 -estradiol or G-1, H1299 cells were counted, cell cycle distribution was detected by flow cytometry, and the activation state of ERK1/2 and the expression of cyclin D1 and P16 protein were detected by Western blot method.Results the expression of GPR30 in adenocarcinoma, low differentiation and stage 鈪，

本文編號：1759191