醫(yī)學(xué)高級職稱論ppt課件(已修改)
2025-01-17 07:53 本頁面
【正文】 5AzaCdR對人食管癌細(xì)胞株生物學(xué)行為及 TFPI2 mRNA表達(dá)的影響 5AzaCdR對人食管癌細(xì)胞株生物學(xué)行為及 TFPI2 mRNA表達(dá)的影響 作者：杜雅冰，邵應(yīng)舉，樊青霞，孫楨，王琳，趙培榮 作者單位：(鄭州大學(xué)第一附屬醫(yī)院腫瘤內(nèi)科，河南鄭州 450002) 【 摘要 】 目的探討 5氮雜 2脫氧胞苷 (5Aza2deoxycytidine,5AzaCdR)干預(yù)對食管鱗癌細(xì)胞株 Eca9706生長增殖及其組織因子途徑抑制物2(tissue factor pathway inhibitor2， TFPI2)基因表達(dá)的影響。方法選取食管鱗癌細(xì)胞株 Eca9706，并用不同濃度的 5AzaCdR處理該細(xì)胞株。MTT法檢測干預(yù)前后細(xì)胞增長率的變化， FCM法檢測干預(yù)前后細(xì)胞凋亡率的變化， RTPCR技術(shù)檢測干預(yù)前后 Eca9706細(xì)胞 TFPI2基因 mRNA的表達(dá)，免疫組化檢測干預(yù)前后 Eca9706細(xì)胞 TFPI2蛋白的表達(dá)。結(jié)果 食管鱗癌細(xì)胞株 Eca9706存在 TFPI2基因超甲基化狀態(tài)，經(jīng) 5AzaCdR處理后，超甲基化狀態(tài)解除，細(xì)胞增殖受到抑制，細(xì)胞凋亡率明顯提高(P)。細(xì)胞中 TFPI2蛋白表達(dá)明顯增強(qiáng)，同時 mRNA的表達(dá)水平也較處理前明顯提高 (P)。結(jié)論 食管癌細(xì)胞系 TFPI2基因超甲基化可抑制其 mRNA表達(dá)，當(dāng)其超甲基化解除后，細(xì)胞增殖受到抑制，同時細(xì)胞凋亡率相應(yīng)提高。 【 關(guān)鍵詞 】 食管癌 。組織因子途徑抑制物 2。5氮雜 2脫氧胞苷 。甲基化 。免疫組化 。逆轉(zhuǎn)錄聚合酶鏈反應(yīng) 。凋亡 ABSTRACT： Objective To explore the effects of 5Aza2deoxycytidine (5AzaCdR) intervention on the growth and proliferation of Eca9706 cell line and protein expression of tissue factor pathway inhibitor2 (TFPI2). Methods Eca9706 cell line was treated by 5azaCdR of different concentrations。 MTT， flow cytometry， immunohistochemistry and RTPCR were used to determine the cell growth， apoptosis， and the expression of TFPI2 gene and its protein. Results Eca9706 cell line had hypermethylation of TFPI2. After demethylation by 5AzaCdR treatment， the proliferation of Eca9706 was inhibited， the apoptosis rate was also increased significantly in the concentrationdependent manner. RTPCR detected that mRNA expression of TFPI2 gene in Eca9706 cell line recovered significantly (P). Conclusion 5AzaCdR can slow the growth of Eca9706 cell， increase the apoptosis rate，
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