缺氧对乳腺癌MDA-MB-231细胞干性的影响

发布时间：2018-05-02 22:36

本文选题：乳腺癌 + 缺氧　；参考：《南华大学》2015年硕士论文

【摘要】：目的:1、通过构建人乳腺癌MDA-MB-231细胞缺氧模型,检测缺氧对MDA-MB-231细胞干细胞标记物表达及自我更新能力、分化的情况,探讨缺氧对MDA-MB-231细胞“干性”调控作用。2、初步探讨Notch信号在缺氧环境下对乳腺癌干细胞“干性”维持的作用方法:1、利用化学制剂二氯化钴(cobalt chloride Co Cl2)诱导,构建人乳腺癌MDA-MB-231细胞缺氧模型。通过Western Blot检测MDA-MB-231细胞中缺氧诱导因子(hypoxia-inducible factor-la,HIF-la)表达情况,验证细胞缺氧模型构建成功。2、缺氧对MDA-MB-231细胞“干性”调节作用:采用平板克隆实验检测细胞的自我更新能力,流式细胞仪检测缺氧对MDA-MB-231的CD44+CD24-/low型细胞的表达情况,免疫印迹试验(Western blot)检测干性标志物蛋白乙醛脱氢酶1(aldehyde dehydrogenase 1ALDH1)的表达情况。3、Notch信号通路在缺氧环境下对乳腺癌干细胞“干性”调节作用的初步研究:采用Western blot检测缺氧对乳腺癌干细胞Notch信号关键分子{Notch1、Hes-1、(Notch intercellular domain NICD)}表达的情况。结果:1、缺氧使MDA-MB-231细胞平板克隆能力明显增强、CD44+CD24-/low细胞比例增多、干性标记物蛋白表达增强。2、缺氧使Notch信号关键分子(Notch1、Hes-1、NICD)在MDA-MB-231细胞中表达增强。结论:1、缺氧可诱导乳腺癌MDA-MB-231干细胞“干性”维持或增强。2、Notch信号通路在缺氧对乳腺癌干细胞“干性”调节作用中发挥着重要作用。
[Abstract]:Objective to construct a hypoxia model of human breast cancer MDA-MB-231 cells to detect the expression of markers, self-renewal ability and differentiation of MDA-MB-231 stem cells induced by hypoxia. To investigate the effect of hypoxia on "dryness" of MDA-MB-231 cells, and to explore the effect of Notch signal on the maintenance of "dryness" of breast cancer stem cells in anoxic environment. The hypoxia model of human breast cancer MDA-MB-231 cells was established. The expression of hypoxia-inducible factor hypoxia-inducible factor-lahla (HIF-laA) in MDA-MB-231 cells was detected by Western Blot. The results showed that the hypoxia model was successfully constructed. The effect of hypoxia on the "dryness" of MDA-MB-231 cells was determined. Flow cytometry was used to detect the expression of hypoxia on CD44 CD24-/low type cells of MDA-MB-231. Western blotting to detect the expression of protein aldehyde dehydrogenase (1(aldehyde dehydrogenase 1ALDH1) in human breast cancer stem cells: a preliminary study on the role of Notch signaling pathway in the regulation of "dryness" of breast cancer stem cells under hypoxia: Western blot was used to detect hypoxia. Expression of Notch signal key molecule {Notch1Hes-1Hes-1 Notch intercellular domain NICD} in breast cancer stem cells. Results at 1: 1, hypoxia significantly increased the percentage of CD44 CD24-/low cells, increased the expression of dry marker protein, and increased the expression of Notch signal key molecule, Notch1Hes-1NICD, in MDA-MB-231 cells. Conclusion: 1, hypoxia can induce MDA-MB-231 stem cells to maintain or enhance the signal pathway of Notch in breast cancer, which may play an important role in the regulation of stem cell dryness by hypoxia.
【学位授予单位】：南华大学
【学位级别】：硕士
【学位授予年份】：2015
【分类号】：R737.9

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