Suppression of renal cell carcinoma growth by inhibition of Notch signaling in vitro and in vivo
J. Clin. Invest. Jonas Sjölund, et al. 118:217 doi:10.1172/JCI32086 [
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Figure 2The Notch signaling pathway is active in CCRCC cells. (
A) Inhibition of the Notch signaling pathway in 786-O cells with a single concentration (10 μM) of the γ-secretase inhibitor DAPT for indicated time periods as monitored by Hes-1 levels. Cells were harvested at indicated time points, and cell lysates were analyzed by immunoblotting. (
B) Inhibition of the Notch signaling pathway in 786-O cells with increasing concentrations of the γ-secretase inhibitor DAPT for 24 hours. Immunoblotting experiments to measure expression levels of the Notch target Hes-1. (
C) The effects of L-685458 and DAPT on Hes-1 protein levels in 786-O cells treated for 24 hours compared with DMSO-treated (–) cells. (
D) DAPT (+) treatment compared with vehicle control (–) treatment of PRC3 and WT7 cells. Cells were harvested after 24 hours of treatment, and cell lysates were analyzed for Hes-1 protein expression. (
E) DAPT (+) treatment compared with vehicle control (–) treatment in a panel of CCRCC cells. Cells were harvested after 24 hours of treatment, and cell lysates were analyzed for Hes-1 protein expression. (
F)
Hes-1 mRNA levels assessed by Q-PCR in DAPT-treated CCRCC cells. Cells were harvested after 24 hours of treatment. DMSO-treated samples were designated as 100%, and data shown are mean + SD of representative experiment performed in triplicate.
