TGF-β-miR-34a-CCL22 signaling-induced Treg cell recruitment promotes venous metastases of HBV-positive hepatocellular carcinoma.
Published
Journal Article
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.
Full Text
Duke Authors
Cited Authors
- Yang, P; Li, Q-J; Feng, Y; Zhang, Y; Markowitz, GJ; Ning, S; Deng, Y; Zhao, J; Jiang, S; Yuan, Y; Wang, H-Y; Cheng, S-Q; Xie, D; Wang, X-F
Published Date
- September 11, 2012
Published In
Volume / Issue
- 22 / 3
Start / End Page
- 291 - 303
PubMed ID
- 22975373
Pubmed Central ID
- 22975373
Electronic International Standard Serial Number (EISSN)
- 1878-3686
Digital Object Identifier (DOI)
- 10.1016/j.ccr.2012.07.023
Language
- eng
Conference Location
- United States