Published online Dec 15, 2001. doi: 10.3748/wjg.v7.i6.816
Revised: July 9, 2001
Accepted: July 16, 2001
Published online: December 15, 2001
AIM: To explore the role of SF/HGF-Met autocrine and paracrine in met astasis of hepatocellular carcinoma (HCC).
METHODS: SF/HGF and c-met transcri ption and protein expression in HCC were examined by RT-PCR and Western Blot in 4 HCC cell lines, including HepG2, Hep3B, SMMC7721 and MHCC-1, the last cell line had a higher potential of metastasis. sf/hgf cDNA was transfected by the method of Lipofectin into SMMC7721. SF/HGF and c-met antibody were used to stimulate and block SF/HGF-c-met signal transduction. Cell morphology, mobility, and proliferation were respectively compared by microscopic observation, wound healing assay and cell growth curve.
RESULTS: HCC malignancy appeared to be relative to its met-SF/HGF expression. In MHCC-1, c-met expression was much stronger than that in other cell lines with lower potential of metastasis and only SF/HG F autocrine existed in MHCC-1. After sf/hgf cDNA transfection or conditioned medium of MHCC-1 stimulation, SMMC7721 changed into elongated morphology, and the abilities of proliferation (P < 0.05) and mobility increased. Such bio-activity could be blocked by c-met antibody (P < 0.05).
CONCLUSION: The system of SF/HGF-c- met autocrine and paracrine played an important role in development and metastas is potential of HCC. Inhibition of SF/HGF-c-met signal transduction system may reduce the growth and metastasis of HCC.