本文選題：IL-37 + 自噬��； 參考：《重慶醫(yī)科大學(xué)》2017年碩士論文

【摘要】：目的:探討IL-37對肝癌細胞自噬的影響及作用機制。方法:CCK-8及流式細胞術(shù)檢測IL-37對肝癌細胞SMMC-7721和Huh-7增殖的影響;在電鏡下觀察自噬體的形態(tài)及數(shù)量;Western blot方法檢測不同濃度IL-37處理的肝癌細胞中自噬蛋白LC3、Beclin1、p62,凋亡蛋白Bcl-2、Bax、Caspase3以及Akt/mTOR信號通路相關(guān)蛋白表達的差異;流式細胞術(shù)檢測肝癌細胞的凋亡水平。結(jié)果:CCK-8結(jié)果顯示IL-37處理組的細胞增殖率降低(p0.01);流式細胞術(shù)結(jié)果顯示IL-37處理使細胞周期中G0/G1期阻滯(p0.01)和凋亡率升高(p0.05);電鏡結(jié)果顯示IL-37處理組自噬體的數(shù)量較對照組明顯升高(p0.01);Western blot結(jié)果顯示IL-37處理組中,LC3-II/LC3-I、Beclin1、Bax、Caspase3的表達均較對照組明顯升高(p0.01),而p62、Bcl-2的表達明顯降低(p0.01),信號通路中p-AKT、p-mTOR及相關(guān)蛋白p-p70S6K和p-4E-BP1的表達明顯降低(p0.01);通過AKT激動劑IGF-1的處理,IL-37可以逆轉(zhuǎn)IGF-1對LC3-II/LC3-I表達的抑制作用。結(jié)論:IL-37處理組中SMMC-7721和Huh-7細胞的增殖活性降低,自噬及凋亡率增高,且IL-37可能通過PI3K/AKT/mTOR信號通路誘導(dǎo)自噬的發(fā)生。本實驗分析了IL-37可能通過促進肝癌細胞自噬和凋亡來降低細胞增殖,這對IL-37的進一步研究及臨床靶向治療有一定的意義。
[Abstract]:Objective: to investigate the effect and mechanism of IL-37 on autophagy of hepatoma cells. Methods the effects of IL-37 on the proliferation of SMMC-7721 and Huh-7 cells were detected by flow cytometry. The morphology and quantity of autophagy were observed under electron microscope. The expression of autophagy protein LC3 / Beclin1 / p62, apoptotic protein Bcl-2 / BaxCaspase3 and Akt / mTOR signaling pathway were detected by Western blot method in different concentrations of IL-37 treated hepatoma cells. Apoptosis level of hepatoma cells was detected by flow cytometry. Results the cell proliferation rate of IL-37 treated group was decreased (p0.01), the cell cycle arrest (p0.01) and apoptosis rate increased (p0.05) after IL-37 treatment, and the number of autophagy in IL-37 treated group was higher than that in control group (p0.05). The results of Western blot showed that the expression of Caspase3 in the IL-37 treated group was significantly higher than that in the control group (p0.01), while the expression of p62mTOR and the associated proteins p-p70S6K and p-4E-BP1 in the signal pathway were significantly decreased (p0.01), and the expression of p-p70S6K and p-4E-BP1 in the signal pathway was significantly lower than that in the control group (p0.01), while the expression of p62mTOR and the associated proteins p-p70S6K and p-4E-BP1 in the signal pathway were significantly lower than those in the control group (p0.01). IL-37 can reverse the inhibitory effect of IGF-1 on LC3-IIR-LC3-I expression. Conclusion the proliferation activity of SMMC-7721 and Huh-7 cells was decreased, the autophagy and apoptosis rate were increased, and IL-37 might induce autophagy through PI3K / AKT / mTOR signaling pathway. In this study, we analyzed that IL-37 may reduce cell proliferation by promoting autophagy and apoptosis of hepatoma cells, which may be of significance for the further study of IL-37 and its clinical targeted therapy.
【學(xué)位授予單位】：重慶醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R735.7

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相關(guān)期刊論文 前1條

1 張國慶;湯成泳;譚婧宇;劉銳;周密;吳忠均;;IL-37抑制體外培養(yǎng)的SMMC-7721肝癌細胞的增殖、侵襲和遷移[J];細胞與分子免疫學(xué)雜志;2015年10期

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本文編號：2109472