Department of Hepatobiliary Surgery, The 3rd Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China.
Acta Biochim Biophys Sin (Shanghai). 2017 Nov 1;49(11):1029-1034. doi: 10.1093/abbs/gmx100.
Angiogenesis plays a key role in the progression of hepatocellular carcinoma (HCC). This study aimed to investigate whether lipopolysaccharide (LPS) could promote HCC angiogenesis and the role of hepatic stellate cell (HSC) in this process. In vivo orthotopic HCC model and the effect of LPS on HSC in vitro were studied. Our results demonstrated that LPS-induced HSC activation during the promotion of HCC growth and angiogenesis in mice. The LPS-TLR4 (Toll-like receptor 4) pathway in HSC is responsible for HCC angiogenesis. LPS-induced secretion of pro-angiogenic factors from HSC could promote endothelial cell migration and tubulogenesis. This study suggests that LPS acts with HSC in tumor stroma and promotes the secretion of pro-angiogenic factors that increase angiogenesis in HCC.
血管生成在肝细胞癌 (HCC) 的进展中起着关键作用。本研究旨在探讨脂多糖 (LPS) 是否能促进 HCC 血管生成以及肝星状细胞 (HSC) 在这一过程中的作用。研究了体内原位 HCC 模型和 LPS 对体外 HSC 的影响。我们的结果表明，LPS 在促进小鼠 HCC 生长和血管生成过程中诱导 HSC 激活。HSC 中的 LPS-TLR4（Toll 样受体 4）通路是 HCC 血管生成的原因。LPS 诱导 HSC 分泌促血管生成因子可促进内皮细胞迁移和管腔形成。这项研究表明，LPS 与肿瘤基质中的 HSC 相互作用，促进促血管生成因子的分泌，从而增加 HCC 的血管生成。
