TLRs、酒精、HCV 和肿瘤发生。
TLRs, Alcohol, HCV, and Tumorigenesis.
机构信息
Department of Molecular Microbiology and Immunology, 503B-HMR, University of Southern California Keck School of Medicine, Los Angeles, CA 90033, USA.
出版信息
Gastroenterol Res Pract. 2010;2010:518674. doi: 10.1155/2010/518674. Epub 2011 Feb 9.
Abstract
Chronic liver damage caused by viral infection, alcohol, or obesity can result in increased risk for hepatocellular carcinoma (HCC). Ample epidemiological evidence suggests that there is a strong synergism between hepatitis C virus (HCV) and alcoholic liver diseases (ALD). The Toll-like receptor (TLR) signaling pathway is upregulated in chronic liver diseases. Alcoholism is associated with endotoxemia that stimulates expression of proinflammatory cytokine expression and inflammation in the liver and fat tissues. Recent studies of HCC have centered on cancer-initiating stem cell (CSC), including detection of CSC in cancer, identification of CSC markers, and isolation of CSC from human HCC cell lines. Synergism between alcohol and HCV may lead to liver tumorigenesis through TLR signaling.
摘要
慢性肝损伤由病毒感染、酒精或肥胖引起，可导致肝细胞癌（HCC）风险增加。大量的流行病学证据表明，丙型肝炎病毒（HCV）和酒精性肝病（ALD）之间存在强烈的协同作用。Toll 样受体（TLR）信号通路在慢性肝病中上调。酒精中毒与内毒素血症有关，后者刺激肝脏和脂肪组织中促炎细胞因子表达和炎症。HCC 的最近研究集中在起始癌症的干细胞（CSC）上，包括在癌症中检测 CSC、鉴定 CSC 标志物以及从人 HCC 细胞系中分离 CSC。酒精和 HCV 之间的协同作用可能通过 TLR 信号导致肝肿瘤发生。
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