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

【摘要】：目的 研究G蛋白耦聯(lián)受體30(GPR30)在非小細(xì)胞肺癌(NSCLC)中的表達(dá)及其與臨床主要病理特征的關(guān)系,并分析GPR30和Ki-67表達(dá)的相關(guān)性,探討雌激素通過(guò)激活GPR30受體信號(hào)途徑調(diào)節(jié)NSCLC增殖的分子機(jī)制。方法 采用免疫組織化學(xué)方法檢測(cè)80例術(shù)后非小細(xì)胞肺癌組織樣本中GPR30和Ki-67的表達(dá)。加入17-β-雌二醇或G-1后,計(jì)數(shù)H1299細(xì)胞,流式細(xì)胞術(shù)檢測(cè)細(xì)胞周期分布,最后通過(guò)Western blot方法檢測(cè)G-1作用后ERK1/2的激活狀態(tài)以及cyclin D1和P16蛋白的表達(dá)。結(jié)果 GPR30更多表達(dá)在腺癌、低分化、Ⅲ期NSCLC腫瘤組織,差異有統(tǒng)計(jì)學(xué)意義(P0.05);GPR30表達(dá)和Ki-67呈中度相關(guān)性(r=0.502,P=0.000)。E2(或G-1)促進(jìn)H1299細(xì)胞增殖,并且更多的細(xì)胞進(jìn)入S期;加入G-1后,磷酸化ERK1/2以及cyclin D1表達(dá)增加,而p16蛋白表達(dá)減少,以上效應(yīng)能被G-15或U0126預(yù)處理2h阻斷。結(jié)論 雌激素通過(guò)激活GPR30-EGFRMAPKs信號(hào)轉(zhuǎn)導(dǎo)途徑促進(jìn)H1299增殖。阻斷GPR30信號(hào)途徑可能成為NSCLC治療的新靶點(diǎn)。
[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(hào)：1759191