PDF(Pubmed)
Abstract：
UNASSIGNED: The crosstalk between hepatocellular carcinoma (HCC) cells and hepatic stellate cells (HSCs) is one of the important mechanisms of liver cancer metastasis. The relationship between liver cancer metastasis and glycolysis has been extensively studied recently. However, the role of von Willebrand factor (vWF) mediated glycolysis mechanism in liver cancer metastasis is currently unknown.
UNASSIGNED: Western blot was used to verify the expression of vWF in HCC cells. PAS staining, glycogen and L-lactate content assays were used to reflect cellular glycolysis levels. The ability of cell migration was explored by Wound-healing and Transwell assays. Besides, the effect of vWF on the progression of HCC in vivo was also studied using subcutaneous xenograft model.
UNASSIGNED: vWF derived from HCC cells promoted tumor migration by mediating glycolysis. Besides, vWF participated in the crosstalk between HCC cells and HSCs. HCC cells activated HSCs through vWF-mediated TGFB1 expression and secretion, and activated HSCs upregulated vWF expression in HCC cells through IL-6 secretion feedback. Further, in vitro and in vivo experiments also confirmed the importance of the JAK1/vWF/TGFB1 axis in regulating HSCs-derived IL-6 mediated HCC migration and growth.
UNASSIGNED: In summary, this article demonstrated that IL-6 released from hepatic stellate cells enhanced glycolysis and migration ability of liver cancer cells by activating JAK1/vWF/TGFB1 axis which may also be a potential target for inhibiting liver cancer metastasis.
UNASSIGNED: Western blot was used to verify the expression of vWF in HCC cells. PAS staining, glycogen and L-lactate content assays were used to reflect cellular glycolysis levels. The ability of cell migration was explored by Wound-healing and Transwell assays. Besides, the effect of vWF on the progression of HCC in vivo was also studied using subcutaneous xenograft model.
UNASSIGNED: vWF derived from HCC cells promoted tumor migration by mediating glycolysis. Besides, vWF participated in the crosstalk between HCC cells and HSCs. HCC cells activated HSCs through vWF-mediated TGFB1 expression and secretion, and activated HSCs upregulated vWF expression in HCC cells through IL-6 secretion feedback. Further, in vitro and in vivo experiments also confirmed the importance of the JAK1/vWF/TGFB1 axis in regulating HSCs-derived IL-6 mediated HCC migration and growth.
UNASSIGNED: In summary, this article demonstrated that IL-6 released from hepatic stellate cells enhanced glycolysis and migration ability of liver cancer cells by activating JAK1/vWF/TGFB1 axis which may also be a potential target for inhibiting liver cancer metastasis.
摘要：
■肝细胞癌（HCC）细胞与肝星状细胞（HSC）之间的串扰是肝癌转移的重要机制之一。肝癌转移与糖酵解之间的关系最近得到了广泛的研究。然而,vonWillebrand因子（vWF）介导的糖酵解机制在肝癌转移中的作用目前尚不清楚。
■Westernblot用于验证vWF在HCC细胞中的表达。PAS染色,糖原和L-乳酸含量测定用于反映细胞糖酵解水平。通过伤口愈合和Transwell测定探索细胞迁移的能力。此外,还使用皮下异种移植模型研究了vWF对体内HCC进展的影响。
■来自HCC细胞的vWF通过介导糖酵解促进肿瘤迁移。此外,vWF参与了HCC细胞与HSC之间的串扰。HCC细胞通过vWF介导的TGFB1表达和分泌激活HSCs，活化的HSCs通过IL-6分泌反馈上调HCC细胞中vWF的表达。Further,体外和体内实验也证实了JAK1/vWF/TGFB1轴在调节HSC来源的IL-6介导的HCC迁移和生长中的重要性。
■总之，本文证明肝星状细胞释放的IL-6通过激活JAK1/vWF/TGFB1轴增强肝癌细胞的糖酵解和迁移能力，这也可能是抑制肝癌转移的潜在靶点。
■Westernblot用于验证vWF在HCC细胞中的表达。PAS染色,糖原和L-乳酸含量测定用于反映细胞糖酵解水平。通过伤口愈合和Transwell测定探索细胞迁移的能力。此外,还使用皮下异种移植模型研究了vWF对体内HCC进展的影响。
■来自HCC细胞的vWF通过介导糖酵解促进肿瘤迁移。此外,vWF参与了HCC细胞与HSC之间的串扰。HCC细胞通过vWF介导的TGFB1表达和分泌激活HSCs，活化的HSCs通过IL-6分泌反馈上调HCC细胞中vWF的表达。Further,体外和体内实验也证实了JAK1/vWF/TGFB1轴在调节HSC来源的IL-6介导的HCC迁移和生长中的重要性。
■总之，本文证明肝星状细胞释放的IL-6通过激活JAK1/vWF/TGFB1轴增强肝癌细胞的糖酵解和迁移能力，这也可能是抑制肝癌转移的潜在靶点。
