SF/HGF-c-Met autocrine and paracrine promote metastasis of hepatocellular carcinoma.
OBJECTIVE
To explore the role of SF/HGF-Met autocrine and paracrine in metastasis of hepatocellular carcinoma (HCC).


METHODS
SF/HGF and c-met transcription 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/HGF 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).


CONCLUSIONS
The system of SF/HGF-c-met autocrine and paracrine played an important role in development and metastasis potential of HCC. Inhibition of SF/HGF-c-met signal transduction system may reduce the growth and metastasis of HCC.
Xie
Q
Q
Experimental Research Center of Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Liu
K D
KD
Hu
M Y
MY
Zhou
K
K
D019898:Autocrine Communication / Q000502:physiology*; D006528:Carcinoma, Hepatocellular / Q000556:secondary*; D017228:Hepatocyte Growth Factor / Q000502:physiology*; D006801:Humans; D008113:Liver Neoplasms / Q000473:pathology*; D019899:Paracrine Communication / Q000502:physiology*; D019859:Proto-Oncogene Proteins c-met / Q000502:physiology*; D014407:Tumor Cells, Cultured
D017228:Hepatocyte Growth Factor; D019859:Proto-Oncogene Proteins c-met