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. Author manuscript; available in PMC: 2012 Jan 9.

Published in final edited form as: Mol Cancer Res. 2010 Aug 24;8(10):1375–1387. doi: 10.1158/1541-7786.MCR-09-0537

Restoration of Smad3 transcriptional activity with inhibition of CDK4 activity. MCF7 (A), T47D (B), and Hs578T (C) study cell lines were transfected with the Smad-responsive CAGA-luc reporter construct, Renilla luciferase reporter, and either wild type (WT) Smad3, 5M Smad3, T178 Smad3 (MCF7 and Hs578T), or T8 Smad3 (T47D only) expression vectors. The cells were treated with vehicle or 800 nM CDK4 inhibitor (CDK4i). Firefly and Renilla luciferase activities were determined. Data are shown as fold increase in normalized luciferase activity (firefly/Renilla) compared with empty vector-transfected MCF7, T47D, or Hs578T cells. Error bars indicate standard deviation from the mean of normalized luciferase activity for each study condition. For Figure 6B * denotes value too low to graphically represent.

Restoration of Smad3 transcriptional activity with inhibition of CDK4 activity. MCF7 (A), T47D (B), and Hs578T (C) study cell lines were transfected with the Smad-responsive CAGA-luc reporter construct, Renilla luciferase reporter, and either wild type (WT) Smad3, 5M Smad3, T178 Smad3 (MCF7 and Hs578T), or T8 Smad3 (T47D only) expression vectors. The cells were treated with vehicle or 800 nM CDK4 inhibitor (CDK4i). Firefly and Renilla luciferase activities were determined. Data are shown as fold increase in normalized luciferase activity (firefly/Renilla) compared with empty vector-transfected MCF7, T47D, or Hs578T cells. Error bars indicate standard deviation from the mean of normalized luciferase activity for each study condition. For Figure 6B * denotes value too low to graphically represent.