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V-4084 inhibits HGF-autocrine GBM proliferation and invasion. a By day 3, U87M2 cells had dispersed significantly (top panel). While V-4084 and its derivative V-837980 significantly inhibited U87MG dispersal at 1 μM, TMZ at 50 μM failed to show any activity. b U87M2 cells constitutively show P-MET, P-MAPK, and activate AKT following HGF. V-4084 inhibited HGF-dependent downstream pathways (MET and MAPK) in U87MG dose-dependently. c To evaluate V4084 efficacy orthotopically, U87M2 cells expressing a luciferase reporter gene (U87M2Luc+) were inoculated into nude mice orthotopically, and tumor growth was monitored by BLI twice a week. V4084 at 30 mg/kg significantly inhibited tumor growth orthotopically (1 week of dosing, one dose per day; p
Although genomic and proteomic tools have been widely used to analyze GBM subtypes [5, 6], to map out specific mutations and signaling pathways [4], or to identify therapeutic targets related in particular to MET and EGFRvIII in combination [11], these approaches have not been used to interpret micro-environmental regulation. The result of using human and mouse arrays to identify the core pathways affected by MET inhibitors in the context of tumor/host crosstalk is speculative but very promising. Although the use of human xenograft tumor models can be debated due to the loss of human host cell biology, in our study, the use of specific human and mouse arrays allows us to measure the signaling pathways impacted in the host and tumor compartments, by which the biological response from host and tumor can be viewed independently. As we have shown, the genes differentially expressed from the human array (n = 550) are very different from those in the mouse array (n = 370), with no overlapping genes. Although nude mice are claimed not to have an intact immune system, we observed pathways such as host-versus-graft disease signaling and antigen presentation to be up-regulated in sensitive xenografts, indicating an increased immune reaction in the host that might be required for treatment efficacy [26]. On the tumor side, all pathways identified were associated with cell-cycle regulation. Strikingly, non-overlapping genes from the tumor and the host still yielded overlapping pathways, with cell-cycle regulation as the common process. Our study, then, uses xenograft mouse models plus human and mouse arrays to provide preliminary, yet important, information about the tumor/host interaction in response to MET inhibitors. Although a more clinically-relevant analysis of tumor/host crosstalk requires the use of orthotopic models, we suggest that for GBM patients in clinical trials, the immune reactions of individual patients might help identify vulnerability to MET inhibitors.
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