SIK2 promotes reprogramming of glucose metabolism through PI3K/AKT/HIF-1α pathway and Drp1-mediated mitochondrial fission in ovarian cancer.
作者:
主题词
动物(Animals);细胞系, 肿瘤(Cell Line, Tumor);细胞增殖(Cell Proliferation);细胞转化, 肿瘤(Cell Transformation, Neoplastic);动力蛋白质类(Dynamins);上皮-间质转化(Epithelial-Mesenchymal Transition);女(雌)性(Female);随访研究(Follow-Up Studies);基因表达调控, 肿瘤(Gene Expression Regulation, Neoplastic);基因敲低技术(Gene Knockdown Techniques);葡萄糖(Glucose);糖酵解(Glycolysis);人类(Humans);缺氧诱导因子1, α亚基(Hypoxia-Inducible Factor 1, alpha Subunit);Kaplan-Meiers评估(Kaplan-Meier Estimate);小鼠(Mice);卵巢肿瘤(Ovarian Neoplasms);卵巢切除术(Ovariectomy);卵巢(Ovary);氧化磷酸化(Oxidative Phosphorylation);磷酸肌醇3-激酶类(Phosphatidylinositol 3-Kinases);预后(Prognosis);原癌基因蛋白质c-akt(Proto-Oncogene Proteins c-akt);信号传导(Signal Transduction);增量调节(Up-Regulation);异种移植模型抗肿瘤试验(Xenograft Model Antitumor Assays)
DOI
10.1016/j.canlet.2019.10.029
PMID
31639424
发布时间
2021-12-04
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Cancer letters
89-101页
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