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TGF-β-miR-34a-CCL22 signaling-induced Treg cell recruitment promotes venous metastases of HBV-positive hepatocellular carcinoma.

ABSTRACT: 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-β 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-β-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.

SUBMITTER: Yang P 

PROVIDER: S-EPMC3443566 | biostudies-literature | 2012 Sep

REPOSITORIES: biostudies-literature

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TGF-β-miR-34a-CCL22 signaling-induced Treg cell recruitment promotes venous metastases of HBV-positive hepatocellular carcinoma.

Yang Pengyuan P   Li Qi-Jing QJ   Feng Yuxiong Y   Zhang Yun Y   Markowitz Geoffrey J GJ   Ning Shanglei S   Deng Yuezhen Y   Zhao Jiangsha J   Jiang Shan S   Yuan Yunfei Y   Wang Hong-Yang HY   Cheng Shu-Qun SQ   Xie Dong D   Wang Xiao-Fan XF  

Cancer cell 20120901 3

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-β 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 im  ...[more]

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