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¹ Jiangsu Key Laboratory for Molecular and Medical Biotechnology, Nanjing Normal University, Nanjing, PR China and ² College of Life Sciences, Anhui Normal University, Wuhu, PR China

Requests for reprints: Chao-Jun Li, Jiangsu Key Laboratory for Molecular and Medical Biotechnology, Nanjing Normal University, Nanjing 210097, PR China. Phone: 86-25-8359-8812; Fax: 86-25-8359-8812. E-mail: licj{at}njnu.edu.cn

c-Met is highly expressed and constitutively activated in various human tumors. We employed adenovirus-mediated RNA interference technique to knock down c-Met expression in hepatocellular carcinoma cells and observed its effects on hepatocellular carcinoma cell growth in vitro and in vivo. Among the five hepatocellular carcinoma and one normal human liver cell lines we analyzed, c-Met was highly expressed and constitutively tyrosine phosphorylated in only MHCC97-L and HCCLM3 hepatocellular carcinoma cells. Knockdown of c-Met could inhibit MHCC97-L cells proliferation by arresting cells at G₀-G₁ phase. Soft agar colony formation assay indicated that the colony forming ability of MHCC97-L cells decreased by 70% after adenovirus AdH1-small interfering RNA (siRNA)/met infection. In vivo experiments showed that adenovirus AdH1-siRNA/met inhibited the tumorigenicity of MHCC97-L cells and significantly suppressed tumor growth when injected directly into tumors. These results suggest that knockdown of c-Met by adenovirus-delivered siRNA may be a potential therapeutic strategy for treatment of hepatocellular carcinoma in which c-Met is overexpressed.

³ http://www.ncbi.nlm.nih.gov/entrez

⁴ http://www.ambion.com/techlib/misc/siRNA_finder.html

Received 4/ 6/05; revised 7/22/05; accepted 8/10/05.