Impact of kinase inhibitors on growth, cell signaling, and survival of Sarc cells. (A) cSarc cells have been exposed to inhibitors (i) of B-cell receptor/BTK-signaling pathway, CCND1-dependent CDK4/6 cell-cycle promoters, or the depicted growth factor receptors and analyzed for cell growth in the MTT conversion assay. (B) Inhibitory effect of FGFR inhibitor on activation of the MEK-ERK and PI3K-AKT signaling pathways using the depicted phospho-specific antibodies. Inhibitors of receptors for PDGF-β, TGF-β, and NGF served as negative controls. (C) Pathway-specific inhibitory effect of the MEK- and PI3K-specific inhibitors on activation of MEK-ERK and PI3K-AKT signaling pathways. (D) FGFR inhibitor-mediated induction of apoptotic cell death as determined by generation of cleaved caspase 3 and PARP. (E) FGFR inhibitor-induced cell death detected by DNA fragmentation (terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling) assay.
Figure 2.

Impact of kinase inhibitors on growth, cell signaling, and survival of Sarc cells. (A) cSarc cells have been exposed to inhibitors (i) of B-cell receptor/BTK-signaling pathway, CCND1-dependent CDK4/6 cell-cycle promoters, or the depicted growth factor receptors and analyzed for cell growth in the MTT conversion assay. (B) Inhibitory effect of FGFR inhibitor on activation of the MEK-ERK and PI3K-AKT signaling pathways using the depicted phospho-specific antibodies. Inhibitors of receptors for PDGF-β, TGF-β, and NGF served as negative controls. (C) Pathway-specific inhibitory effect of the MEK- and PI3K-specific inhibitors on activation of MEK-ERK and PI3K-AKT signaling pathways. (D) FGFR inhibitor-mediated induction of apoptotic cell death as determined by generation of cleaved caspase 3 and PARP. (E) FGFR inhibitor-induced cell death detected by DNA fragmentation (terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling) assay.

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