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This study evaluates the impact of Foretinib on the phosphorylation levels of key signaling molecules including VEGFR-2, PDGFR-β, c-Met, Akt, and ERK1/2 in 21-0208 HCC cells. These cells, derived from HCC21-0208 tumors, were treated with varying concentrations of Foretinib for 24 hours. The subsequent Western blot analysis demonstrated significant alterations in phosphorylation, as indicated by fold changes relative to controls. Results were consistent across experiments, highlighting Foretinib's potential effects on these pathways in cancer therapy.
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PDGF-Rβ p-PDGF-Rβ(Tyr1021) Fold 1 0.8* 0.4** 0.3** 0.1*** p-VEGFR-2(Tyr951) Fold 1 0.5* 0.3* 0.2** 0.1*** VEGFR-2 p-Gab-1(Tyr627) Fold 1 0.12* 0.01* 0.01* 0.01* Gab-1 p-Met(Tyr1003) Fold 1 0.3* 0.2** 0.1*** 0.1*** c-Met p-ERK½ Fold 1 0.85 0.5* 0.3** 0.2** ERK1 p-Akt(Ser473) Fold 1 0.6* 0.2** 0.1** 0.2** Akt Fig 1S.Effects of foretinib on the phosphorylation levels of VEGFR-2, PDGFR-, c-Met, Akt and ERK1/2 in 21-0208 HCC cells. 21-0208 HCC cells were isolated from HCC21-0208 tumors and cultured as described in Materials and Methods. They were treated with 0, 0.5, 1, 1.5 and 2 μM of foretinib in DMEM containing 1% FBS for 24 hours. Lysates from vehicle- and foretinib-treated tumors were subjected to Western blotting described in Materials and Methods. Blots were incubated with the indicated antibodies. Representative Western blots and quantification analysis expressed as fold of controls are shown. Different asterisks (*) indicate significantly different from one another at P <0.05. Experiments were repeated at least twice with similar results. Cleaved PARP Fold 1 3.6* 3.9* 8.5** 18.9*** Foretinib (µM) 0 0.5 1 1.5 2
