NANOG 依赖性代谢重编程和肿瘤起始干细胞样细胞的对称分裂。
NANOG-Dependent Metabolic Reprogramming and Symmetric Division in Tumor-Initiating Stem-like Cells.
机构信息
Southern California Research Center for ALPD and Cirrhosis, Los Angeles, CA, USA.
Department of Molecular Microbiology and Immunology, Los Angeles, CA, USA.
出版信息
Adv Exp Med Biol. 2018;1032:105-113. doi: 10.1007/978-3-319-98788-0_8.
Abstract
Alcohol abuse synergistically heightens the development of the third most deadliest cancer hepatocellular carcinoma (HCC) in patients infected with hepatitis C virus (HCV). Ectopically expressed TLR4 promotes liver tumorigenesis in alcohol-fed HCV Ns5a or Core transgenic mice. CD133+/CD49f + tumor-initiating stem cell-like cells (TICs) isolated from these models are tumorigenic have p53 degradation via phosphorylation of the protective protein NUMB and its dissociation from p53 by the oncoprotein TBC1D15. Nutrient deprivation reduces overexpressed TBC1D15 in TICs via autophagy-mediated degradation, suggesting a possible role of this oncoprotein in linking metabolic reprogramming and self-renewal.
摘要
酒精滥用会协同作用，加重丙型肝炎病毒 (HCV) 感染患者中第三大致命癌症——肝细胞癌 (HCC) 的发展。异位表达的 TLR4 促进了酒精喂养的 HCV Ns5a 或 Core 转基因小鼠的肝肿瘤发生。从这些模型中分离出的 CD133+/CD49f+肿瘤起始干细胞样细胞 (TICs) 具有致瘤性，通过磷酸化保护性蛋白 NUMB 及其与 p53 分离的致癌蛋白 TBC1D15 降解 p53。营养剥夺通过自噬介导的降解减少 TIC 中过表达的 TBC1D15，提示该致癌蛋白在连接代谢重编程和自我更新中可能起作用。
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本文引用的文献
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NANOG Metabolically Reprograms Tumor-Initiating Stem-like Cells through Tumorigenic Changes in Oxidative Phosphorylation and Fatty Acid Metabolism.NANOG通过氧化磷酸化和脂肪酸代谢的致瘤性变化对肿瘤起始干细胞样细胞进行代谢重编程。
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Reciprocal regulation by TLR4 and TGF-β in tumor-initiating stem-like cells.TLR4 和 TGF-β 在肿瘤起始干细胞样细胞中的相互调节作用。
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