RT Journal Article
SR Electronic
T1 Effects of the augmenter of liver regeneration on the biological behavior of hepatocellular carcinoma
JF Saudi Medical Journal
JO Saudi Med J
FD Prince Sultan Military Medical City
SP 1001
OP 1009
VO 30
IS 8
A1 Tang, Lin
A1 Sun, Hang
A1 Zhang, Lin
A1 Deng, Jian C.
A1 Guo, Hui
A1 Zhang, Ling
A1 Liu, Qi
YR 2009
UL http://smj.org.sa/content/30/8/1001.abstract
AB OBJECTIVE: To take advantage of the small interfering ribonucleic acid (siRNA) targeting the human augmenter of liver regeneration (hALR) and anti-hALR monoclonal antibody (McAb) to inhibit the function of hALR, and to demonstrate whether the growth of hepatoma is influenced by siRNA targeting hALR and anti-hALR McAb through inhibiting expression of hALR.METHODS: This study was conducted in the Key Laboratory of Molecular Biology for Infectious Diseases, Ministry of Education, Institute for Viral Hepatitis, Chongqing Medical University, China, between January 2005 and May 2007. We transfected siRNA plasmid pSIALR-A, which targeted the complementary deoxyribonucleic acid (cDNA) of hALR and the unrelated control plasmid pSIALR-B into human hepatocellular liver carcinoma cell line (HepG2) cells. Then, the proliferation of HepG2 cells, after being treated with pSIALR-A and anti-hALR McAb was detected. The growth of the xenograft tumor was observed after being treated with pSIALR-A and anti-hALR McAb in nude mice.RESULTS: We successfully constructed expressing plasmid pSIALR-A and pSIALR-B. The pSIALR-A inhibited the expression of hALR in HepG2 cells significantly. The siRNA targeting hALR and anti-hALR McAb inhibited obviously the growth of HepG2 cells in vitro. siRNA targeting hALR and anti-hALR McAb significantly inhibited the growth of xenograft tumor in 5 nude mice. Anti-hALR McAb inhibited apparently the autonomous growth of HepG2 cells.CONCLUSION: Our results demonstrated that anti-hALR McAb inhibited the autonomous growth of hepatoma cells obviously, moreover, hALR maintained the autonomous growth of hepatoma cells in vitro through an autocrine mechanism.