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NQO1/PKLR通过糖代谢重编程调控乳腺癌演进的机制研究

中文摘要第6-10页
ABSTRACT第10-15页
ABBREVIATIONS第18-20页
1. INTRODUCTION第20-37页
2. MATERIALS AND METHODS第37-50页
    2.1 Materials第37-39页
        2.1.1 Experimental reagents and instruments第37-39页
    2.2 Methods第39-50页
        2.2.1 Cell culture第39-40页
        2.2.2 Cell viability assay第40页
        2.2.3 Transtection第40-41页
        2.2.4 Stable cell line generation第41页
        2.2.5 TCGA BC cohorts第41页
        2.2.6 Wound healing assay第41-42页
        2.2.7 Colony-forming assay第42页
        2.2.8 EdU assay第42-43页
        2.2.9 Immunofluorescence第43页
        2.2.10 Migration assay第43页
        2.2.11 Invasion assay第43-44页
        2.2.12 Western blot第44-45页
        2.2.13 Immunohistochemistry第45页
        2.2.14 Measurement of glucose, lactate, and ATP第45-46页
        2.2.15 Co-Immunoprecipitation (Co-IP)第46-47页
        2.2.16 In vivo tumorigenesis and metastasis assays第47-48页
        2.2.17 Statistical analysis第48-50页
3. RESULTS第50-81页
    3.1 NQO1 overexpression correlates with poor prognosis in BC第50-55页
    3.2 NQO1 enhances tumor growth and in vivo tumorigenesis第55-59页
    3.3 NQO1 induces epithelia-mesenchymal transition and promotes cellular migration and invasion第59-65页
    3.4 NQO1 promoted BC cell growth and metastasis via regulating glycolysis reprogramming第65-71页
    3.5 Identification of PKLR as a target gene of NQO1 in BC第71-74页
    3.6 The NQO1/PKLR axis regulated the AMPK and AKT/mTOR pathways to modify BC EMT and glycolysisreprogramming第74-78页
    3.7 PKLR is inversely correlated with the expression of NQO1 in normal and breast cancers第78-81页
4. DISCUSSION第81-88页
5. CONCLUSIONS第88-89页
REFERENCES第89-105页
攻读博士学位期间取得的科研业绩第105-106页
致谢第106页

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