Author/Authors :
Yang، نويسنده , , Pengyuan and Li، نويسنده , , Qi-Jing and Feng، نويسنده , , Yuxiong and Zhang، نويسنده , , Yun and Markowitz، نويسنده , , Geoffrey J. and Ning، نويسنده , , Shanglei and Deng، نويسنده , , Yuezhen and Zhao، نويسنده , , Jiangsha and Jiang، نويسنده , , Shan-Shan and Yuan، نويسنده , , Yunfei and Wang، نويسنده , , Hong-Yang and Cheng، نويسنده , , Shu-Qun and Xie، نويسنده , , Dong and Wang، نويسنده , , Xiao-Fan، نويسنده ,
Abstract :
Summary
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.
