發(fā)布時(shí)間：2018-04-03 12:24

  本文選題：人喉癌　切入點(diǎn)：SOX　出處：《中國醫(yī)科大學(xué)學(xué)報(bào)》2014年03期

【摘要】：目的探討5-氟尿嘧啶(5-FU)對(duì)人喉癌Hep-2細(xì)胞中干細(xì)胞轉(zhuǎn)錄因子SOX2表達(dá)的影響及機(jī)制,并分析SOX2拮抗5-FU誘導(dǎo)的細(xì)胞凋亡作用。方法 CCK-8法檢測48 h內(nèi)不同濃度5-FU對(duì)Hep-2細(xì)胞生長的抑制作用,統(tǒng)計(jì)抑制率和IC50值。Western blot法檢測5-FU作用不同時(shí)間后SOX2的表達(dá)量,并檢測PI3K/AKT信號(hào)活化情況。Hoechst染色法檢測細(xì)胞凋亡。結(jié)果5-FU對(duì)Hep-2細(xì)胞生長抑制作用明顯,IC50值為20.92μg/mL。隨著時(shí)間的延長SOX2表達(dá)增高,48 h達(dá)到最大值,磷酸化AKT活化也隨著時(shí)間的延長逐漸增加。使用PI3K/AKT信號(hào)特異性抑制劑LY294002處理后,SOX2表達(dá)被下調(diào);Hoechst染色法顯示細(xì)胞凋亡數(shù)增多。同時(shí)檢測凋亡相關(guān)蛋白表達(dá)變化,結(jié)果顯示Survivin、Bcl-2、BAX在5-FU處理的Hep-2細(xì)胞中表達(dá)均上升,但PI3K/AKT信號(hào)抑制后抗凋亡蛋白Survivin、Bcl-2被顯著下調(diào),凋亡蛋白BAX表達(dá)繼續(xù)上調(diào)。結(jié)論 PI3K/AKT信號(hào)活化誘導(dǎo)SOX2表達(dá)在Hep-2細(xì)胞拮抗5-FU誘導(dǎo)的細(xì)胞凋亡中發(fā)揮了重要作用。
[Abstract]:Objective to investigate the effect and mechanism of 5-fluorouracil (5-FU) on the expression of transcription factor SOX2 in human laryngeal carcinoma Hep-2 cells, and to analyze the effect of SOX2 on the apoptosis induced by 5-FU.Methods CCK-8 assay was used to detect the inhibitory effect of 5-FU at different concentrations on the growth of Hep-2 cells within 48 h. The expression of SOX2 was detected by IC50 value. Western blot assay was used to detect the expression of SOX2 and the activation of PI3K/AKT signal. Hoechst staining was used to detect the apoptosis of Hep-2 cells.Results the inhibitory effect of 5-FU on the growth of Hep-2 cells was found to be 20.92 渭 g / mL.The expression of SOX2 increased to the maximum at 48 h, and the activation of phosphorylated AKT increased with the prolongation of time.After treated with PI3K/AKT signal specific inhibitor LY294002, the expression of SOX2 was down-regulated by Hoechst staining.At the same time, the expression of apoptosis-related protein was detected. The results showed that the expression of survivin Bcl-2mBAX increased in 5-FU treated Hep-2 cells, but the anti-apoptotic protein survivin Bcl-2 was significantly down-regulated and the expression of apoptotic protein BAX continued to up-regulate after PI3K/AKT signal suppression.Conclusion SOX2 expression induced by PI3K/AKT signal activation plays an important role in Hep-2 cells antagonizing apoptosis induced by 5-FU.
【作者單位】： 中國醫(yī)科大學(xué)附屬第一醫(yī)院耳鼻咽喉科;
【基金】：遼寧省自然科學(xué)基金(201202287)
【分類號(hào)】：R739.65

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