Liver Cancer
Copyright ©2005 Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. May 7, 2005; 11(17): 2564-2569
Published online May 7, 2005. doi: 10.3748/wjg.v11.i17.2564
Alpha-fetoprotein triggers hepatoma cells escaping from immune surveillance through altering the expression of Fas/FasL and tumor necrosis factor related apoptosis-inducing ligand and its receptor of lymphocytes and liver cancer cells
Meng-Sen Li, Qiu-Ling Ma, Qian Chen, Xin-Hua Liu, Ping-Feng Li, Guo-Guang Du, Gang Li
Meng-Sen Li, Qiu-Ling Ma, Qian Chen, Department of Biochemistry, Hainan Medical College, Haikou 571101, Hainan Province, China
Xin-Hua Liu, Ping-Feng Li, Guo-Guang Du, Gang Li, Department of Biochemistry and Molecular Biology, Peking University Health Science Center, Beijing 100083, China
Author contributions: All authors contributed equally to the work.
Correspondence to: Dr. Gang Li, Department of Biochemistry and Molecular Biology, Peking University Health Science Center, Beijing 100083, China. mengsenli@163.com
Telephone: +86-10-82802891
Received: June 7, 2004
Revised: June 8, 2004
Accepted: June 17, 2004
Published online: May 7, 2005
Abstract

AIM: To investigate the mechanism of α-fetoprotein (AFP) in escaping from the host immune surveillance of hepatoc-ellular carcinoma.

METHODS: AFP purified from human umbilical blood was administrated into the cultured human lymphoma Jurkat T cell line or hepatoma cell line, Bel7402 in vitro. The expression of tumor necrosis factor related apoptosis-inducing ligand (TRAIL) and its receptor (TRAILR) mRNA were analyzed by Northern blot and Western blot was used to detect the expression of Fas and Fas ligand (FasL) protein.

RESULTS: AFP (20 mg/L) could promote the expression of FasL and TRAIL, and inhibit the expression of Fas and TRAILR of Bel7402 cells. For Jurkat cell line, AFP could suppress the expression of FasL and TRAIL, and stimulate the expression of Fas and TRAILR. AFP also could synergize with Bel7402 cells to inhibit the expression of FasL protein and TRAIL mRNA in Jurkat cells. The monoclonal antibody against AFP (anti-AFP) could abolish these functions of AFP.

CONCLUSION: AFP is able to promote the expression of FasL and TRAIL in hepatoma cells and enhance the expression of Fas and TRAILR in lymphocytes. These could elicit the escape of hepatocellular carcinoma cells from the host’s lymphocytes immune surveillance.

Keywords: Alpha-fetoprotein; Hepatocellular carcinoma; Immune escape