Stromal cells paracrinously regulate the c-met transcript in VMR tumor cells of different in metastatic potential

The c-met protooncogene, which codes for tyrosine protein kinase, was shown to be more intensely transcribed in highly metastatic tumor VMR-P than in low-grade VMR-0. The gene for the hepatocyte growth factor (HGF), a c-Met ligand, was transcribed in VMR-P but not in VMR-0 tumor. The content of the c-met mRNA was the same andHGF was not transcribed in VMR-0 and VMR-P cells culturedin vitro. Thus, the difference between VMR-P and VMR-0 tumors was attributed to interactions of tumor and stromal cells. Thein vitro coculturing of tumor cells and fibroblasts confirmed paracrine regulation of c-met transcription.