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  • Title: Participation of c-met in the progression of human gastric cancers: anti-c-met oligonucleotides inhibit proliferation or invasiveness of gastric cancer cells.
    Author: Kaji M, Yonemura Y, Harada S, Liu X, Terada I, Yamamoto H.
    Journal: Cancer Gene Ther; 1996; 3(6):393-404. PubMed ID: 8988842.
    Abstract:
    The protooncogene c-met encodes the receptor for hepatocyte growth factor (HGF), a potent epithelial cell mitogen with scattering activity. In this study, we first screened c-met expression in human gastric carcinomas. Twenty-eight of 154 tumors (18%) were positively stained for MET proteins. The incidence of c-met expression increased with higher histopathological stages of the cancer. Second, we examined functional roles of c-met in cultured gastric carcinoma cells, using an antisense strategy. Cell lines used were MKN-45, TMK-1, and MKN-28. Among them, MKN-45 cells exhibited the highest c-met expression and grew in response to HGF, whereas TMK-1 cells had an ability to invade in an HGF-dependent manner. When antisense oligodeoxyribonucleotides complementary to c-met messenger RNA (mRNA) were administered to the culture medium, the content of MET protein was selectively decreased in either MKN-45 or TMK-1 cells, indicating that the antisense molecules did inhibit the translation of c-met mRNA. The growth of MKN-45 cells was markedly inhibited by the antisense c-met oligonucleotides in a dose-dependent manner, but not by sense or scrambled controls. The antisense oligonucleotides also effectively inhibited the migration of TMK-1 cells. These results indicate that c-met gene products may be causally related to the proliferation or invasion of gastric cancer cells, and that antisense c-met DNA has the potential to help circumvent the progression of gastric cancers.
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