Journal
CANCER CELL
Volume 22, Issue 3, Pages 291-303Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2012.07.023
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Funding
- American Cancer Society [RSG-10-157-01-LIB]
- Ministry of Science and Technology Key Program of China [2012ZX10002009-017]
- National Basic Research Program of China [2010CB912102]
- National Cancer Institute of the National Institutes of Health [CA151541]
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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-beta 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-beta-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.
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