TGF-¦Â-miR-34a-CCL22 Signaling-Induced Treg Cell Recruitment Promotes Venous Metastases of HBV-Positive Hepatocellular Carcinoma

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• 作者：Pengyuan Yang ; Qi-Jing Li ; Yuxiong Feng ; Yun Zhang ; Geoffrey?J. Markowitz ; Shanglei Ning ; Yuezhen Deng ; Jiangsha Zhao ; Shan Jiang ; Yunfei Yuan ; Hong-Yang Wang ; Shu-Qun Cheng ; Dong Xie ; Xiao-Fan Wang
• 刊名：Cancer Cell
• 出版年：2012
• 出版时间：11 September, 2012
• 年：2012
• 卷：22
• 期：3
• 页码：291-303
• 全文大小：5876 K

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Summary

Portal vein tumor thrombus (PVTT) is strongly correlated to a poor prognosis for patients with hepatocellular carcinoma (HCC). In this study, we uncovered a causative link between hepatitis B virus (HBV) infection and development of PVTT. Mechanistically, elevated TGF-¦Â activity, associated with the persistent presence of HBV in the liver tissue, suppresses the expression of microRNA-34a, leading to enhanced production of chemokine CCL22, which recruits regulatory T (Treg) cells to facilitate immune escape. These findings strongly suggest that HBV infection and activity of the TGF-¦Â-miR-34a-CCL22 axis serve as potent etiological factors to predispose HCC patients for the development of PVTT, possibly through the creation of an immune-subversive microenvironment to favor colonization of disseminated HCC cells in the portal venous system.